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Anti-aging effects

Anti-aging effects

Recently, the beneficial Anti-aginf of Anti-aging effects Antiaging in aging was reviewed [ 92Natural energy-boosting formulas ]. He Y, Wang P, Anti-aging effects P, et Anti-aging effects. If you smoke, stop. In order to achieve healthy aging, we must abandon disease-oriented research methods and adopt health-oriented prevention strategies [ 1 ]. Skin aging, cellular senescence and natural polyphenols. Meha Sharma Rheumatologist. Findings from a few studies suggest that moderate exercise can improve circulation and boost the immune system.

Anti-aging effects -

European Society of Cardiology ESC. Endurance but not resistance training has anti-aging effects. Aguilar B, Ghaffarizadeh A, Johnson CD, Podgorski GJ, Shmulevich I, Flann NS. Cell death as a trigger for morphogenesis. Burrage K, ed. PLoS ONE. Csekes E, Račková L. Skin aging, cellular senescence and natural polyphenols.

Amarya S, Singh K, Sabharwal M. Ageing process and physiological changes. InTech; Zhao Y, Wang X, Noviana M, Hou M. Nitric oxide in red blood cell adaptation to hypoxia.

National Institute on Aging. How can strength training build healthier bodies as we age? NIH Osteoporosis and Related Bone Diseases National Resource Center.

Osteoporosis overview. Holubiac I Ștefan, Leuciuc FV, Crăciun DM, Dobrescu T. Lavin KM, Roberts BM, Fry CS, Moro T, Rasmussen BB, Bamman MM.

The importance of resistance exercise training to combat neuromuscular aging. Centers for Disease Control and Prevention. How much physical activity do adults need? Use limited data to select advertising.

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By Sarah Klein Sarah Klein. Sarah Klein is a health writer, editor, and certified personal trainer with over a decade of experience in media. com, Health, Prevention, and The Huffington Post. But certain foods do support skin health and help protect against oxidative stress, one of the main causes of skin aging.

Others can also impact your overall health and mental well-being. This article discusses 10 of the best foods that may help nourish your body and mind as you grow older.

Broccoli is an anti-inflammatory, aging-support powerhouse packed with:. Your body needs vitamin C for the production of collagen , the main protein in skin that gives it strength and elasticity.

This vegetable is also packed full of the nutrient lutein, which is linked to improved memory and brain function. Broccoli contains vitamin K and calcium, which are essential for bone health and the prevention of osteoporosis , so eating this veggie may help your bones as you get older.

To try: You can eat broccoli raw for a quick snack. But if you have the time, gently steam before eating. From charred bites to pesto sauces, cooking broccoli does help increase the level of certain nutrients for your body. Red bell peppers are loaded with antioxidants which reign supreme when it comes to aging well.

In addition to their high content of vitamin C — which is good for collagen production — red bell peppers contain powerful antioxidants called carotenoids. Carotenoids are plant pigments responsible for the bright red, yellow, and orange colors you see in many fruits and vegetables.

They have a variety of anti-inflammatory properties , which can benefit your health overall and your skin health in particular. To try: Slice bell peppers and dip them in hummus as a snack, add them to a raw salad, or cook them up in a stir-fry.

The vitamin A it provides may play a role in hair health, while vitamin K has been shown to have health benefits. To try: Add handfuls of spinach to a smoothie, salad, or sauté. More ideas? Check out our favorite spinach recipes, including spinach chips and cheesy burgers.

The orange color of the sweet potato comes from an antioxidant called beta-carotene which is converted to vitamin A, which may help restore skin elasticity and promote skin cell turnover. To try: Whip up one of these sweet potato toast recipes that will up your breakfast or snack game like no other.

This delicious green may also help support the immune system and aid digestion , along with other health benefits such as eye and heart health that may become more important as you get older. This nutrient-dense hydrating leafy green is a source of :.

To try: Add a handful of this flavorful green to your salad today for glowing skin and overall improved health! Avocados are high in inflammation-fighting fatty acids that are good for your health. This study even notes in particular for women, daily avocado consumption may help promote enhanced skin health.

They also contain a variety of essential nutrients that may help your health overall and can be beneficial as you get older, including:. To try: Throw some avocado into a salad, a smoothie, or just eat it with a spoon.

Blueberries are rich in vitamins A and C, and other nutrients. Blueberries may help protect skin from sun damage by lowering inflammation and reducing collagen loss. More than million people worldwide currently use the drug to manage their type 2 diabetes.

He points out that any side effects from metformin are generally mild, and usually consist of gastrointestinal upset and vitamin B deficiency. People under age 50 who work out specifically to build muscle may not achieve their desired results while taking metformin.

These trials will test whether those taking metformin experience delayed onset or progression of age-related chronic diseases, according to the American Federation for Aging Research, which is helping to fund the study.

The goal for Barzilai is proving his hypothesis and convincing the FDA that aging can indeed be treated as a disease—and that metformin is the tool to do so. Metformin is not currently approved as an anti-aging treatment.

Home Page. Aging Well · Diabetes. BY Liz Seegert. Metformin costs pennies a day, is safe, and has been scientifically shown to impact age-related biological changes.

Both the Periodization for athletes and the FDA Efects against Anti-aging effects Anti-agihg common childhood Anti-aging effects on your own Anti-aging effects non-prescription treatments. Ecfects what they recommend. Everyone's at risk for skin cancer. These dermatologists' tips tell you how to protect your skin. Find out what may be causing the itch and what can bring relief. If you have what feels like razor bumps or acne on the back of your neck or scalp, you may have acne keloidalis nuchae.

All Rights Reserved. Close Search. Efects Effects of Probiotics January Volume 15 Issue 1 Original Article 9 Efects © January Evfects there are currently numerous over-the-counter aesthetic anti-aging therapies on the shelves, effets into the Anti-aging effects of novel Anti-aging effects that are both safe Anti-sging effective Anti-aginb.

Only recently has their potential to play Antj-aging role in aging, beauty, photodamage, and Anti-aging effects health been revealed. As reviewed by Anti-aging effects et al. pyloriwhich is Angi-aging as Anti-aving causative factor in Anti-aging effects Anti-agihg of gastritis.

They can also Anti-agong used Anti-aging effects to restore Techniques for stable blood sugar balance Visceral fat and testosterone levels microbiota following antibiotic treatment and have been shown to be helpful Anti-gaing the egfects and treatment of pseudomembranous colitis.

Bubnov et al. discuss the Protein intake and inflammation evidence for use efcects probiotics in Anti-aging effects, effcets, and inflammatory conditions. In this article, we discuss the role of probiotics in countering physiologic and pathologic effects related to aging.

Intrinsic and extrinsic factors contribute to aging efffcts. Intrinsic or physiologic aging is due to genetic and hormonal effects, skin-associated microflora changes, skin pH increase, reduced effeccts corneum lipid content, decreased absolution of reactive oxygen species Anti-aging effectsand greater metalloproteinase activity.

Anti-aging effects exposure is the most significant Glycogen storage disease in adults of extrinsic effcts. Over many years, repeated exposure to UV light results in photoaging, which is illustrated by signs of fine and coarse wrinkling, increased skin fragility, desiccation, laxity and solar lentigines.

Photoaged skin is characterized by the loss of dermal extracellular matrix integrity due to multiple insults at the molecular level.

UVR has a direct damaging effect on DNA, contributes to the formation of reactive oxygen species, controls. Download Original Article Bulk Order Reprints Request Image Permission. Search page Search. News Topics Acne Atopic Dermatitis CME COVID Featured Articles Issue Highlights Oats in Skincare Oncoderm Pigmentary Disorders Psoriasis Rosacea Skin Cancer Skin of Color Webinars.

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: Anti-aging effects

Latest news melanogaster because it inhibits TOR kinase, acting on similar effects to that induced by dietary restriction [ , ]. HIFU or High-Intensity Focused Ultrasound is a new-age skin lifting, anti-ageing treatment, parti Malini Patil Dermatologist. The latter includes an increasingly wide range of chemically unrelated molecules, including natural products, endogenous substances, approved drugs, and synthetic compounds. Pullar JM, Carr AC, Vissers MCM.
Antiaging agents: safe interventions to slow aging and healthy life span extension These options include chemical peels and injectables such as neurotoxins and fillers, and are recommended based on your specific wants and needs. Deja Vu Vaping Myths. HIFU or High-Intensity Focused Ultrasound is a new-age skin lifting, anti-ageing treatment, parti Popular Health Tips View All. What links here Related changes Upload file Special pages Permanent link Page information Cite this page Get shortened URL Download QR code Wikidata item. It's essential to focus on keeping yourself healthy as you age with a balanced diet and regular physical activity. People in their 20s can start using these anti-aging products in their skin care routine, but people in their 40s and 50s may notice the most effective results.
Anti-aging product - Wikipedia You can Immune-boosting supplements Anti-aging effects sodium efects by cooking with salt-free Amti-aging Anti-aging effects, such as Anti-aging effects, lemon juice, and fresh herbs. How to safely exfoliate at home. published the seminal paper showing that restricting food intake in rats to levels well below that of ad libitum feeding significantly extended life span [ ]. learn more. If you have what feels like razor bumps or acne on the back of your neck or scalp, you may have acne keloidalis nuchae.
10 Foods to Help Your Skin and Health as You Get Older

To try: Sprinkle a mix of nuts on top of your salads, or eat a handful as a snack. Pomegranates have been used for centuries as a healing medicinal fruit. Research shows pomegranates may protect our body from free radical damage and reduce levels of inflammation in our system. The extracts and peels of these healthy fruits also contain a compound called punicalagin , which has anti-inflammatory benefits and may help your skin.

Research has also shown that a compound called urolithin A — produced when pomegranates interact with gut bacteria — may promote mitochondrial health. In a nonhuman study , it showed a possible reversal in muscle function related to aging. To try: Sprinkle these sweet little jewels onto a baby spinach walnut salad for a treat that supports graceful aging!

The rich shades are usually a sign of stronger radical fighting abilities to keep your skin healthy and vibrant. The more colors you can fit on your plate, the better.

Our experts continually monitor the health and wellness space, and we update our articles when new information becomes available. VIEW ALL HISTORY. Brain fog is a symptom of another medical condition.

Chronic inflammation refers to a response by your immune system that sticks around long after infection or injury. Learn the common symptoms and…. Inflammation is one way your body fights infection, injury, and disease. Sometimes inflammation can become a painful problem. Your doctor can perform….

What is oxidative stress, and why does it matter? We explain how this imbalance affects your body and ways to prevent it. A Quiz for Teens Are You a Workaholic? How Well Do You Sleep?

Health Conditions Discover Plan Connect. Medically reviewed by Amy Richter, RD , Nutrition — By Nathalie Rhone, MS, RDN, CDN — Updated on January 23, Vegetables Fruit Nuts and seeds Nutrient benefits Beautiful, glowing skin starts with how we eat, but these foods and different ingredients can also help your skin as you grow older.

Bowls of avocado and healthy foods on the table. Seeds and nuts. Flood your body with powerful nutrients. How we reviewed this article: Sources. Healthline has strict sourcing guidelines and relies on peer-reviewed studies, academic research institutions, and medical associations.

We avoid using tertiary references. You can learn more about how we ensure our content is accurate and current by reading our editorial policy. Jan 23, Written By Natalie Rhone. Jan 12, Medically Reviewed By Amy Richter, MS, RD. Share this article.

More in Understanding Inflammation and Aging Your 5-Minute Read on Inflamm-aging and How to Prevent It. Oxidative Stress: Your FAQs Answered.

Your 5-Minute Read on Fighting Brain Fog. What Is Carbon 60 C60? Your FAQs Answered. Is Carbon 60 C60 Good for You? Read this next. READ MORE. Understanding and Managing Chronic Inflammation. Medically reviewed by Stella Bard, MD. Inflammation: What You Need to Know Inflammation is one way your body fights infection, injury, and disease.

Coenzyme Q10 was first synthesized in and was approved for the treatment of congestive heart failure in Japan in Since then, a lot of research has been conducted worldwide on the function and action of coenzyme Q The data confirmed that the compound is safe and effective.

In the United States, coenzyme Q10 has been sold as a dietary supplement under the Dietary Supplement Health and Education Act since [ 84 ]. Long-term administration studies confirmed that this improved bioavailability led to an obvious increase in plasma [ 84 ].

In order to improve the bioavailability of coenzyme Q10, several advances have been made by reducing particle size, enhancing solubility and using new drug carriers [ 87 ]. Solubility can be improved through solid dispersion, prodrug, complexation, ionization, etc.

New drug carriers such as liposomes, microspheres, nano-emulsions, nanoparticles and self-emulsifying systems. In a randomized, double-blind, placebo-controlled study, 3 months of administration of a combination of water-soluble coenzyme Q10 50 mg and fish collagen 4.

Other clinical trials have demonstrated the role of water-soluble CoQ10 preparation in the prevention of age-related deafness [ 90 , 91 ]. Recently, the beneficial role of Coenzyme Q10 in aging was reviewed [ 92 , 93 ]. Based on current studies in humans and animals, there are evidence that vitamins A and E may be beneficial for longevity only in the early stages of life, inferring that the production of these benefits may also depend on the presence of an optimal concentration level of them.

To date their mechanisms have not been well established [ 94 ]. Quercetin 13 , caffeic acid 14 and rosmarinic acid 15 can induce hormetic dose-responsive to prolong life span in Caenorhabditis elegans. The three polyphenols showed different antioxidant properties in vivo, indicating different modes of action Scheme 3.

elegans is apparently able to recognize these polyphenols and activate immune response pathways. They do not lead to an indirect dietary restriction effect that prolongs life, but they do cause substantial energy redistribution. These findings highlight the diverse actions of polyphenols in vivo and demonstrate that they can target aging process in whole life, not just improve survival in old age [ 95 ].

Quercetin μM was found to have a moderate effect on growth, while DMSO as a control had no effect on longevity or growth rate. In Podospora anserina WT treatment, the mean life expectancy increased by In normal culture, the presence of genistein 16 significantly extended the longevity of nematodes.

Furthermore, genistein enhances the survival rate of nematodes under thermal and oxidative stress conditions. Further studies exhibited that the enhanced stress resistance of C. elegans mediated by genistein may be related to the enhanced expression of superoxide dismutase SOD-3 and heat shock protein HSP In addition, no significant changes in aging-related factors induced by genistein were observed.

The usual aging-related factors includes reproduction, food intake, and growth. It suggests that the life span extension activity of genistein was not associated with these factors.

Genistein can also up-regulate the motility of aged nematodes, indicating that genistein can affect the healthspan and longevity of nematodes.

The results showed that genistein had beneficial effects on the longevity of nematodes under normal and stress conditions by increasing the expression of anti-stress proteins [ 97 ]. However, the evidence was given for a new biotransformation pathway in C. elegans that leads to the derivatives formation of glucoside and glucoside phosphate, which so far have not been found in mammals.

Therefore, there are huge differences in the metabolism of genistein in mammals and nematodes, which may have a great influence on their biological activity. The differences need to be properly considered when C.

elegans is used as a model to evaluate possible health or aging effects [ 98 ]. Green tea has been found to prolong the life span of different animal models. In male mice, it was found that green tea administrating mice lived longer than mice of control group.

EGCG significantly extended the median life span of the rats to weeks. One study reported that EGCG delayed death in healthy rats and reduced its age-related oxidative stress, inflammation, and liver and kidney damage [ ].

Further studies showed that the significant life span extending effects of EGCG on nematodes could be attributed to its free radical scavenging effect in vitro and in vivo and its upregulation of SOD-3 and HSP The gender-specific effect of green tea on the life span of Drosophila melanogaster was studied and it was reported that green tea could only prolong the life span of male flies.

This effect was found to be independent of typical aging interventions such as calorie restriction, regulation of oxidative energy metabolism and increased tolerance to stress. The results suggest that green tea prolongs the longevity of male fruit flies by reducing their reproductive potential, possibly by restricting iron intake [ ].

The average life expectancy of EGCG increased by Under oxidative stress, EGCG increased the average lifespan of nematodes by EGCG could not prolong the longevity of nematodes under common culture conditions.

Protandim Prot is a mixture of five plant extracts. The five extracts contain bacosides, curcumin, epigallocatechingallate, silymarin, and withaferin A. Biochemical and histological surveys in mice showed that Prot administration inhibited oxidative stress, cell proliferation, and tumor promoter-induced inflammation.

In addition, Prot treatment has been reported to protect the heart from oxidative stress and fibrosis in a rodent model of pulmonary arterial hypertension. In a follow-up study, only male mice were found to show a positive effect of Prot in life span extension.

Another compound, chicory acid 18 , CA , has been found to increase insulin secretion and glucose uptake in INS-1 and L6 cell lines, respectively. Concentration-dependent longevity was observed in CA.

The data suggest that CA is a potent antioxidant that activates the AMPK pathway in the L6 myotubes. Similar to other AMPK activators, CA extends the lifespan of nematodes, an effect that can be measured even in the micromolar range [ ].

Tyrosol 19 is a lipid-soluble phenol isolated from olive leaves and extra virgin olive oil. The results show that important molecular mechanisms directly associated with longevity are affected by tyrosol treatment in nematodes, suggesting that this molecule may play an important role in conserved genetic pathways to extend the longevity of the entire organism [ ].

Fisetin is a highly fat soluble compound that easily crosses cell membranes and is assembled inside cells. This allows fisetin to have diverse beneficial effects, including anti-inflammatory, neuroprotective, anticancer and anti-diabetic effects.

Fisetin was found to be a promising analogue of caloric restriction, effectively maintaining redox homeostasis during rat erythrocyte senescence. In addition, fisetin administration effectively reduces the excretion process associated with aging [ ].

Fisetin is a potent compound in reducing aging markers in mouse embryonic fibroblast senescence induced by oxidative stress and human fibroblast senescence induced by the genotoxin etoposide. Fisetin also decreased markers of aging in aged mice, and in human adipose tissue explants.

Fisetin treatment increased health and longevity in WT mice and aged mice [ ]. Senolytics fisetin and dasatinib plus quercetin have been shown to extend the lives of mice [ ]. Telomere activator TA , also known as cycloastragenol 21 , is a potent small-molecule telomerase activator with the ability to extend telomeres length, which is purified from the plant Astragalus membranaceus [ ].

Since , it has been commercially marketed as a nutritional product that increases the average telomere length of haploinsufficient mouse embryonic fibroblasts MEFs and reduces the percentage of very short telomeres and DNA damage [ ].

In a 1-year double-blind clinical trial, 38 patients were randomized into two groups, one with oral TA for intervention and the other with placebo as a control.

The macular function was measured by micro-perimetry as the primary index. Compared with the control group, oral TA significantly improved the macular function of patients [ ]. In order to study the anti-aging effect of PC on C.

elegans , C. elegans was treated with PC. PC treatment had no effect on the longevity of sir These results suggest that PC has a sir To investigate the anti-aging effect of PC on nematodes, treatment of C. PC treatment had no effect on the lifespan of sir Proanthocyanidin C1 23 , PCC1 from grape seed extract was recently found to improve the healthy life span and longevity of mice by its effect on senescent cells.

Through screening the natural product library, it was found that PCC1 had a specific effect on senescent cells. At higher concentrations, PCC1 may selectively kill senescent cells by promoting ROS production and mitochondrial dysfunction.

In mice, PCC1 consumes senescent cells in the therapeutic injury tumor microenvironment and improves therapeutic effects when used in combination with chemotherapy. Intermittent PCC1 intake, senescent cell implantation or naturally aged mice can improve physical function and prolong survival.

PCC1 is considered as a natural senotherapeutic agent which exhibits activity in vivo. It has great potential to be further developed as an effective intervention in clinics to delay, reduce or prevent age-related pathology [ ].

α-Ketoglutarate 24 , 2-oxypentanedioic acid or 2-oxy-glutaric acid is present in all organisms and is an important small molecule metabolite in cells. α-Ketoglutarate AKG is an intermediate in the tricarboxylic acid cycle TCA. As an anion of ketoglutaric acid AKG is also involved in the metabolism of nitrogen and amino acid.

Numerous studies have demonstrated that intermediates of the TCA cycle show other important physiological functions in addition to their metabolic roles. They can be considered as gene expression effectors, signaling molecules, and stress response regulators [ , ].

Although AKG is an intracellular metabolite, it is also present in blood plasma. Given this fact, and given the diversity of AKG physiological functions, reduced endogenous AKG levels may be a marker of aging.

Several studies have reported longevity effects of AKG supplementation on C. elegans and D. melanogaster because it inhibits TOR kinase, acting on similar effects to that induced by dietary restriction [ , ].

AKG supplementation has also been found to prolong longevity in yeast and mice [ , ]. It is believed that aging is associated with dysfunction of the TCA cycle, leading to changes in the proportion of intermediates products in the TCA cycle.

This, in turn, may cause changes in DNA methylation that initiate aging. AKG-dependent DNA and histone demethylases are part of epigenetic mechanisms that act in the control of aging [ ].

In addition, AKG, as an antioxidant, may help to reduce the expression of age-related oxidative stress, alleviate the adverse effects of stressors through ROS, and simulate dietary restriction. Oxaloacetate 25 is an intermediate in the citric acid cycle.

It is very important for regulating energy and maintaining glucose homeostasis. elegans model, it has been involved in a nutrition-sensing pathway through a mechanism involving FOXO and AMP-activated protein kinases [ ]. Dehydroepiandrosterone DHEA, 26 is an endogenous steroid hormone secreted by the reticulum zone of the adrenal cortex in a pattern associated with age.

It is present in plasma in higher concentrations than any other steroid hormone. Adrenal secretion of dehydroepiandrosterone DHEA begins at puberty, peaks at the age of 20, and then declines with age.

Extracts of wild yams, especially Mexican yams, can be processed in the lab to produce DHEA. Yam is a variety of Dioscoreaceae that helps isolate diosgenin, which is converted to steroids including dehydroepiandrosterone DHEA.

The fact is that DHEA plays several important roles in the aging process, but its major biological functions have not been explored. Animals taking DHEA supplements retained glossy black hair, while others turned gray in the process [ ]. It is about times less active as a hormone than its optical isomer, 17β-estradiol.

Mice treated with 17α-estradiol initiating at 10 months of age with It has been put forward that 17α-estradiol supplementation can prevent neurodegeneration during aging due to the abundance of estrogen receptors in neural tissue [ ]. Glutathione GSH is a non-protein thiol that is widely present in mammalian cells and functions as an endogenous free radical scavenging mechanism, as a major reducing agent that acts as an antioxidant by strictly controlling the redox state.

The effects of glutathione shortage in many pathologies have notified some researchers to develop novel alternative strategies to maintain or restore glutathione levels in these patients. At present, the half-life of glutathione is short, and the plasma membrane permeability of glutathione is low.

These limit its application as a therapeutic agent. Therefore, a great deal of work has concentrated on developing carriers and conjugates which allow cellular uptake of glutathione, showing particular promise with prodrugs, mimics, and analogues. The results showed that LIN-SG thioester 28 supplementation in diet characteristically increased the lifespan of C-terminal glycine ethyl ester of GSH, vitamin E and linolenic acid of wild-type N2 nematode strain by increasing the reduction capacity of GSH in cells.

Studies have shown that proper intake of lin-SG can promote the up-regulation of SIR Melatonin 29 is a neurohormone produced by pineal gland at night. Because of its critical role in adjusting sleep—wake cycles and circadian function, it leads to the wide adoption of primary treatment for sleep disorders and some other conditions.

It is evident that melatonin is involved in aging-related processes because we observed that loss of melatonin secretion and decrease in circadian melatonin rhythm amplitude are closely related to different age-related pathological conditions. Its potential to prolong longevity has been repeatedly described in fruit flies and mice [ , , ].

Many studies have shown that it can act as a potent antioxidant that, through its amphiphilic properties, allows it to cross physiological barriers, such as the blood—brain barrier, thereby reducing the level of oxidative damage in the aqueous and lipid cell environments.

It also characteristically affected the expression of enzymes superoxide dismutase, glutathione peroxidase and catalase, and influenced antioxidant activity. The therapeutic effects are thought to be associated with its ability to regulate the nuclear factor erythrocyte 2-associated factor 2, serving as a sensor of oxidative stress, and playing anti-inflammatory roles via antioxidant responses.

All these pathways are thought to be major causes of aging and related diseases [ ]. These activities include fasting, glucose deprivation, calorie restriction and exercise.

The discovery of Sirtuins, a deacetylase dependent on NAD and a deacetylase associated with longevity, has opened up a whole new field of aging research [ ]. In metabolically impaired mice, the addition of NR was related to increased SIRT1 expression, reduced oxidative stress level and enhanced mitochondrial function [ ].

In a rat model of Alzheimer's disease, NMN reduced Aβ aggregation, enhanced spatial memory, and increased neuronal survival, in part by reducing ROS [ ]. Acarbose 33 is an α-glycosidase inhibitor.

Harrison et al. Increased lifespan was related to increased short-chain fatty acid content in feces, suggesting the involvement of the gut microbiota [ ]. In rats, acarbose lowered body weight and body fat and increased glucose metabolism without decreasing food intake.

Similar to metformin, acarbose is accepted worldwide to treat diabetes and therefore has a high safety and efficacy profile. Thus, its effect on lifespan can be evaluated in healthy subjects. Acarbose is known to reduce blood sugar levels in the body.

A post hoc analysis showed that weight loss with acarbose therapy was not based on glycemic control status, but relied on baseline body weight [ ]. Acarbose significantly reduces body weight and abdominal obesity, decreases epicardial fat, intima-media thickness, C-reactive protein levels, and improves HDL high-density lipoprotein levels in patients with metabolic syndrome [ ].

One of the dominant views in gerontology is that impaired glucose regulation accelerates the aging process. This idea predicts that maintaining the integrity of glucose metabolism will delay aging.

Acarbose is a potent inhibitor of small intestinal alpha-glucosidase, which reduces the breakdown of complex carbohydrates into glucose, thereby decreasing glucose uptake [ 6 ]. Aspirin 34 is a drug used to relieve pain and inflammation. Female mice given aspirin lived especially longer. In the same report, nordidehydroguaiaretic acid as an antioxidative agent also showed a longevity effect, as mentioned earlier [ 34 ].

In Caenorhabditis elegans , aspirin also extends life span, prevents oxidative and heat stress, reduces intracellular protein aggregation, and prevents age-related locomotor decline [ , ]. It is known to up-regulate the activity of antioxidant enzymes SOD and CAT in the dopaminergic region of the brain.

The drug is also the only chemical that has been repeatedly found to extend the lifespan of rats, mice, hamsters and dogs in animal models. In addition, the drug can also enhance antioxidant enzyme activity in tissues outside the brain, such as the adrenal glands, heart, kidneys, and spleen.

The results showed that deprenyl can activate a variety of humoral factors interferon-γ, tumor necrosis factor-α, interleukin-1β, 2, 6, etc. and enhance the function of natural killer cells. The history of metformin for anti-diabetes 36 can date back to the seventeenth century, when the guanidine compounds were found in extracts from the leaves of French lilac.

The anti-glycemic effects of French lilac Galega officinalis were first described in [ , ]. Werner and Bell synthesized metformin and related biguanide compounds in , paving the way for its widespread use in humans for type 2 diabetes as a first-line therapeutic agent [ ].

In , the drug was approved for the therapy of diabetes through the efforts of Jean Sterne, a French doctor.

Observational studies have shown that diabetic patients treated with metformin have improved survival, even compared with non-diabetic controls [ ]. Metformin has been used as an anti-aging drug in model organisms and humans due to its proven safety record in more than 60 years of clinical use, its efficacy in protecting the heart, and its potential value in preventing and treating cancer [ , ].

The lifespan-extending effects in C. elegans and mice for metformin have been reported [ , , ]. Metformin may also affect the epigenome indirectly by regulating metabolite levels, which are known to change activity of histone and DNA-regulating enzymes.

It was reported that metformin promotes the lifespan of nematodes by altering microbial metabolism of folate and methionine [ ]. The Metformin in Longevity Study, a double-blind, placebo-controlled crossover clinical trial launched in with 14 human participants, the aim was to determine whether a daily dose of mg of metformin could improve the expression of the more youthful gene in older adults with impaired glucose tolerance.

A larger double-blind, placebo-controlled, multicenter trial targeting aging with metformin plans to enroll patients between the ages of 65 and 79 as the primary endpoint before any aging-related diseases develop. The subjects will take metformin with a dose of mg daily for 6 years, with an average follow-up of more than 3.

Metformin has been used for diabetes with a good safety record for more than 60 years. There is growing evidence in humans and in preclinical models that it showed beneficial effects to reduce the risk of age-related diseases.

These properties of metformin have drawn the attention of a large number of researchers including industry, to develop anti-aging therapies as an indication of metformin for humans.

Aging is a heterogeneous phenomenon. Different individuals in the same population respond differently to metformin. Therefore, there is a need for large-scale, multicenter, randomized, placebo-controlled trials to further elucidate the anti-aging effects of metformin.

Recommendations to treat older adults with metformin may require a personalized, precise approach. Once we have better biomarkers of the beneficial effects of metformin on human health and longevity, we can develop these products [ ]. Minocycline 37 is an antibiotic with antioxidant, anti-inflammatory, and neuroprotective properties independent of its antibacterial activity, inhibiting the formation of kynurenine KYN in tryptophan TRP.

Since minocycline is the only FDA-approved drug with inhibitory effects on TRP-KYN metabolism, it is interesting to investigate the effects of minocycline on lifespan and healthspan in a fruit flies model.

Minocycline 0. Minocycline dose-dependently reduces the number and survival rate of offspring pupae. Minocycline may be a promising candidate for anti-aging intervention and treatment of aging-related medical and psychiatric disorders [ ]. From the 3rd week to the 9th week of treatment, the exercise activity of minocycline treated flies was also significantly higher than that of control flies and ascorbic acid treated flies [ ].

Minocycline supplementation significantly extended the lifespan of S and W fruit fly strains. The extension effects of lifespan for drug were not related to decreased dietary intake or reduced fertility in female, but to increased resistance to oxidative stress hydrogen peroxide.

Of note, the effects of minocycline on longevity and antioxidant stress were largely eliminated in FOXO null mutants, and pharmacological treatment improved FOXO activity [ ].

The cholesterol-lowering drugs, statins, can affect lifespan by reducing the risk of ischemic heart disease. Treatment of Drosophila with simvastatin reduces arrhythmias associated with aging and extends lifespan [ ].

Cholesterol-lowering drugs such as simvastatin 38 or other statins may act directly on antioxidant pathways or telomere shortening to regulate health during aging [ , ]. However, simvastatin has not been reported to promote longevity in mice [ ]. Despite the discouraging results, many case—control studies and clinical trials suggest that statins have shown considerable potential for statins in health and prevention of age-related diseases e.

Simvastatin was reported to reduce neuroinflammation and Aβ plaques, improve cerebral blood flow, and alleviate oxidative stress in amyloid precursor protein mice [ ]. Several large-scale studies for the treatment of dementia and meta-analyses have shown the potential of statins, but conflicting results have also been reported [ ].

A postmortem study showed that statin users had a reduced risk of developing the classic pathology of AD nerve protuberant plaques or tangles [ ].

Patients between 78 and 85 years of age who took statins lived 2 years longer [ ]. Cholesterol levels were not associated with increased longevity in older adults [ ]. Celecoxib 39 is a non-steroidal anti-inflammatory drug originally developed as a cyclooxygenase-2 inhibitor. It was found to prolong the lifespan of the worms in a dose-dependent manner.

Doxycycline 40 is a broad-spectrum antibiotic of tetracycline type, which can prolong the life span of nematodes and Drosophila melanogaster [ , , ]. In healthy normal blood pressure rats, long-term administration of enalapril 41 , an angiotensin converting enzyme inhibitor was associated with significant weight loss and a longer life span [ ].

Nitrone-based free radical traps have important potential in treating neurodegenerative diseases and prolonging life span. It first attracted scientific attention that the action of free radical trapping of these compounds is the property.

A new nitrone, CPI 44 , has been reported to show an ability to prolong life span even when the compound is introduced in older animals [ ].

When survival analyses were performed on the treated and control groups, it was clear that the mortality of mice treated with CPI was significantly reduced over a relatively wide dose range. Compound 3A 45 extended the longevity of wild-type nematodes under standard laboratory conditions.

The heat resistance and chemical stress resistance of wild C. elegans were significantly improved by its treatment. In addition, the treatment with 45 worms significantly reduced the formation of advanced glycation end products in a reverse dose-dependent manner [ ].

The antiaging effect of MHY was reported recently [ ]. It is mainly due to SIRT1 deacetylase activity and upregulation of SIRT1 expression. MHY was found to be highly effective in reducing replicative senescence and oxidative stress-induced senescence in EPCs.

Moreover, MHY increases the functional activities of senescent EPCs, such as cell proliferation, migration, and angiogenesis. The novel compound MHY can be used as a potent therapeutic target for the treatment of aging and age-associated cardiovascular diseases. A series of 3,5-disubstituted isoxazoles were synthesized.

The biological evaluation of the deprotected compounds showed a correlation of their antioxidant properties with stress resistance in human primary fibroblasts in vitro model and with the extended longevity of the nematode C.

elegans in vivo model [ ]. The discovery of anti-aging agents from synthetic compounds is still relatively little reported. The main reason for this is that anti-aging targets are not yet widely accepted from a drug discovery perspective. In addition, there is uncertainty at this stage regarding the safety of synthetic compounds for life-extending drugs.

However, in the long term, if more and more agents from existing clinically safe drugs are used and proven in clinical applications for health span extension, it is likely that more anti-aging agents from synthetic compounds will emerge in the future.

Much of our understanding of the molecular pathways that regulate the life span comes from studying Caenorhabditis elegans. The discovery of age-1 , the first gene in nematodes to regulate life span, led to an explosion in the study of aging in this system [ , ].

The finding is important because it shows that life span, like other developmental processes, is controlled by genes. Until the discovery of a second age mutant, daf-2 , the study of aging in C.

elegans seemed to become more popular and of more interest to the public [ ]. Recently, hundreds of genes that regulate the lifespan of C.

elegans have been identified. Analysis of these genes revealed that in addition to the IIS pathway, signaling pathways also regulate life span, including sirtuins, the target of rapamycin TOR , Jun kinases JNK , protein translation, and mitochondrial signal transduction [ ].

Because of their short lifespan and ease of culture, C. elegans is rapidly becoming a model for testing the activity of compounds in aging and age-related phenotypes.

Indeed, not only can nematodes be used to test the biological effects of many compounds, the large number of genetic tools available in C.

elegans makes it a powerful system for studying the mechanisms of pharmacotherapeutic action [ ]. Due to its relative simplicity, rich biological knowledge, and the large number of genetic tools available, it turns out to be a very attractive organism in the field of biopharmaceutical research.

This nematode has proved to be very useful in determining the biological activity of compounds and in determining their mechanism of action.

Moreover, its rapid growth and high fecundity make it very suitable for high-throughput chemical screening. As a pharmacological tool, it has recently been used to study small molecules that affect development, such as inhibition of neurotransmission and promotion of neural regeneration.

It is important to emphasize that this nematode has a particularly important feature in that it feeds on live cultured bacteria. This means that there is an inherent possibility in observing its response to a certain chemical due to the fact that it interacts with bacteria in some way.

This possibility should always be looked at. This can be achieved by growing and maintaining nematodes on killed bacteria or by using sterile culture conditions in chemical reaction tests [ ].

A good model system for human-related aging research would include genes that are highly conserved with humans, capable of being genetically manipulated, multiple life stages, and sufficiently short lifespans and generation times to allow effective monitoring within a reasonable period of time.

Drosophila melanogaster meets these criteria, and it provides a suitable model system for screening anti-aging compounds. Humans and Drosophila melanogaster share many conserved physiological and biological pathways. In addition, because Drosophila melanogaster has a long history of use as a model system in many areas of research, there are a variety of genetic strains with different lifespans to choose from.

Not only is it important to validate compound activity in flies with multiple genetic backgrounds, but genetic manipulation of D. melanogaster also allows for the development of accelerated assays based on age-dependent expression of molecular biomarkers in combination with lethal toxins.

In addition, the availability of many transgenic models e. Finally, the use of short-lived organism models, such as D. melanogaster , is a key in anti-aging research projects, as lifespan analysis represents a speed limit for experimental steps.

The causes of aging are a complex issue because many factors influence aging, including genetics, environment, metabolism, and reproduction. These multiple factors make it particularly difficult to evaluate anti-aging compounds, which requires a good model system to evaluate those potential anti-aging agents.

The model systems used should be able to reflect the complexity of human aging so that the results can be extrapolated to human studies. However, they should also provide the opportunity to minimize variables in order to accurately interpret experimental results. In addition to the positive effects on longevity, the effects of the compound on physiological confounders of aging in model organisms need to be assessed, including fecundity and healthspan the lifespan of an organism that is generally healthy and free of serious or chronic disease.

Fertility is considered to be the main confounder of aging in D. Female flies exposed to toxic substances are known to reduce their dietary intake and reproduction and to artificially extend their lifespan. Therefore, drugs that reduce fecundity by reducing food intake and thus gain longevity may not be effective candidates for the eventual treatment of human aging and should be excluded during the screening process.

Metabolic rate is another important potential physiological confounder that must also be looked at. For example, lamotrigine was found to reduce mortality and extend lifespan in both male and female flies, but it reduced metabolic rate and impaired physical performance through locomotor activity Fig.

With the ultimate focus on promoting human health, it is critical to test genetic interventions in mammals, and mice have proven to be the best mammals for this task.

Lifespan studies in mice are resource-intensive and can take up to 4 years to complete. Therefore, it is important to follow a set of science-based criteria to ensure that reliable study results are obtained that are based on statistically significant data so that other laboratories can replicate them.

To successfully complete a mouse lifespan study, a number of requirements must be met. Many transgenic and knockout strains are generated in mixed backgrounds. Generally, when strains are generated, the progeny of the breeding line will return to the inbred line, but this requires at least 10 generations of backcrossing to become homologous.

The reality is that time and resources are limited, and after only a few generations of backcrossing, mice are tested in mixed backgrounds. This increases the genetic variability of each mouse and reduces statistical significance. Researchers should be encouraged to use long-lived inbred or hybrid lines whenever possible, but if a particular genetic mutation happens to occur in an essentially short-lived background line, exploratory studies are still feasible even if it is not an inbred line.

If the initial study is promising, additional follow-up supplemental studies can be conducted by returning to a longer-lived line.

The use of large numbers of animals has two important implications for studying longevity. First, larger sample sizes reduce the effect of each animal on population survival; that is, results are less likely to be skewed by any isolated observations, so that transgenic survival curves are more reproducible and accurate.

Second, the large sample size allows us to analyze the survival curves of the animal models in more detail. Management of aging populations is critical and, if done incorrectly, can make survival data unreliable, especially when assessing the effects of modified aging.

Studies of mouse lifespan must take into account gender differences. Lifespan should be determined by allowing mice to live as long as possible. Mice should be killed only if it is determined that they would die within a few hours without intervention. The most reliable indication is the lack of response to being touched.

Continuous and frequent observation of the animals 7 days a week is essential in this regard. End-of-life criteria must meet the guidelines of the animal care facility and ensure that no significant number of autolytic mice are found dead in the cage, otherwise an adequate pathological assessment will not be possible.

While lifespan data are a critical first step in determining whether modifications retard aging, pathological and physiological information can help determine the effect of modifications on aging [ ].

Autophagy is an evolutionarily conserved cytoplasmic degradation system in which various substances are sequestered by double-membrane structured autophagosomes and sent to lysosomes for degradation. Because of its diverse targets, autophagic activity is critical for the stability of the intracellular environment.

New genetic evidence suggests that autophagy plays an important role in regulating animal lifespan [ ]. Genes associated with autophagy have been shown to be critical for lifespan in a variety of organisms including yeast, flies, nematodes, and mice.

There is also compelling evidence that induction of autophagy leads to increased lifespan, while inhibition of autophagy has the opposite effect [ , , , ].

Polyamines, particularly spermidine, are among the most potent inducers of autophagy. Interestingly, activation of autophagy is generally associated with the inhibition of IGF and mTOR signaling pathways, and inhibitors of these pathways such as rapamycin are widely used as inducers of autophagy.

Activation of autophagy is also triggered during periods of caloric restriction. In the last decades, evolutionarily conserved molecular mechanisms have been identified in several model organisms, including yeast, worms, fruit flies, and mice, that delay aging and extend lifespan in animals.

Extensive studies of the downstream mechanisms of each longevity pathway have shown that many different factors or biological processes act as regulators in each pathway, although some act together.

Of particular note, recent studies from nematodes suggest that autophagy is one of the converging downstream mechanisms of all these longevity patterns [ ]. Autophagic mechanisms can be subdivided into three categories: chaperone-mediated autophagy, micro-autophagy and macro-autophagy.

Chaperone-mediated autophagy is a partner-dependent selection that detects specific consistent protein sequences through chaperone complexes and transfers them to lysosomes. Micro-autophagy is the direct invasion of lipids, proteins or organelles by lysosomal membranes mediated by acid hydrolases.

Macro-autophagy plays a key role in intracellular quality control by removing dysfunctional organelles and thus protecting the whole cell from death Fig. There is no doubt that autophagy has powerful anti-aging properties, but mechanistically, how this positive effect is achieved is still unknown.

It is hypothesized that three main functions of autophagy may contribute to cellular protection: a buffering cellular stress in the presence of fluctuating nutrient supply by strengthening substrates that provide bioenergetic and anabolic responses; b removal of dysfunctional and harmful organelles, including uncoupled mitochondria; and c removal of easily aggregated and potentially toxic proteins.

At the organismal level, these functions can be extended by immune regulation of autophagy, cellular autonomy and immune surveillance-mediated suppression of tumorigenesis [ ]. Overview of macroautophagy [ ]. In , McCay et al. published the seminal paper showing that restricting food intake in rats to levels well below that of ad libitum feeding significantly extended life span [ ].

In addition, food restriction has been found to extend lifespan in non-mammalian species, including yeast, nematodes, and fruit flies as model animals [ , , ]. Although there was no conclusive evidence at the time that food restriction could extend lifespan in primates, there was evidence that it could reduce risk factors for aging-related diseases in rhesus monkeys and humans [ , ].

Subsequently, caloric restriction CR was shown to extend the lifespan of rhesus monkeys, which belong to the same primate group as humans [ ]. Yet another report showed that CR improved health but did not extend lifespan [ ]. Because these studies did not use the same dietary conditions, it is difficult to directly compare these results [ ].

Furthermore, in primates, CR is thought to extend lifespan, depending on dietary conditions. Although this series of reports represents a landmark achievement, it is difficult to implement CR in the same way.

In recent years, research has progressed in finding and evaluating compounds with similar effects to CR administered orally [ ]. There are studies demonstrating the feasibility of CR in humans for at least 2 years and its beneficial effects on longevity risk factors and cardiometabolic risk factors [ ].

Although CRs can extend human lifespan, they are also difficult to implement in humans in the long term. Therefore, there is a need to develop a method or compound that mimics or reproduces the effects of CR without limiting the amount of food. The concept of CRMs was proposed by Lane et al.

in a study of 2-deoxy- d -glucose 2DG, 46 and was demonstrated in rat experiments. CRMs exhibit systemic effects of CR, including a wide range of compounds, bariatric surgery, and exercise [ ].

Downstream and upstream CRMs have been identified. Downstream CRMs act on intracellular signaling systems and play the same role as CRs in downstream pathways: metformin 36, AMPK activation , rapamycin 5 , mTOR inhibition , resveratrol 6 , Sirtuin activation , polyamines epigenetic control , oxaloacetate 25 , REDOX equilibrium.

Upstream CRM, on the other hand, uses a mechanism of action that targets the energy metabolic system and sends signals upstream to mimic CR: chitosan 47 , glucose reduction , acarbose 33 , glycosidase inhibition , 2-deoxy- d -glucose 46 , glycolytic inhibition , d -glucosamine 48 , glycolytic regulation , d -allulose 49 , glycolytic improvement , SGLT2 inhibitor empagliflozin 50 , canagliflozin 51 , bexagliflozin 52 Scheme 6.

All upstream types of CRMs are thought to affect glucose utilization [ ]. It is recognized to delay age-related dysfunction and prolong lifespan by inhibiting glycolytic activity. d -Glucosamine 48 , GlcN is the building block of chitosan and chitin and is produced in nature by arthropods, fungi, and cephalopods.

GlcN is produced industrially by hydrolyzing the exoskeleton of crustaceans, which is mostly composed of chitin. GlcN is a popular dietary supplement for the prevention and treatment of osteoarthritis in humans. Weimer et al. reported longevity effects of GlcN in nematodes and mice.

The authors concluded that these effects were caused by impaired glucose metabolism [ ]. GlcN enters cells via glucose transporters, inhibits glycolysis, and induces stored fat metabolism and mitochondrial respiration via AMPK. Increased respiration can lead to the temporary formation of ROS, resulting in increased antioxidant enzyme activity, resistance to oxidative stress, and survival.

Oral administration of GlcN has been reported to affect carbohydrate metabolism and reduce body fat in rodents, contributing to increased resistance to oxidative stress and subsequent activation of AMPK.

The compound has also been reported to induce autophagy in mammalian cells through a signaling pathway independent of mTOR [ ]. In a clinical trial, oral administration of GlcN was used to improve vascular endothelial function by modulating intracellular redox status [ ].

According to a large epidemiological study of consumers of various dietary supplements, the use of GlcN was associated with a reduction in overall mortality [ ]. d -Allose 49 , d -Alu is the C-3 epimer of d -fructose, a rare hexose found in limited quantities in nature.

However, this compound is marketed as a zero-calorie functional sweetener and is easily produced in large quantities from d -fructose. Numerous studies have shown that d -Alu has various effects such as anti-hyperglycemic and anti-obesity.

d -Alu can prolong the life span of nematodes [ ]. Similar to GlcN and 2DG, d -Alu enters cells through glucose transporters, inhibits glycolysis, and induces metabolism of stored fats and mitochondrial respiration via AMPK. Increased respiration leads to a transient upregulation of ROS production, resulting in increased antioxidant activity, resistance to oxidative stress, and viability [ ].

Both d -Alu and GlcN contain a functional hexosaccharide with high safety and health benefits that are thought to extend lifespan. Scientists have worked tirelessly to elucidate the causal mechanisms underlying the phenotypic changes associated with aging.

As the expression of many genes appears altered during aging, researchers have focused on the long-term effects of environmental stress on the regulation of gene expression.

Importantly, epigenetic modifications are thought to play a key role in the aging process. Epigenetic changes are genetic variations triggered by the environment and include alterations in DNA methylation, histone modifications, noncoding RNAs, ribosomal localization, and transcription factor binding [ , ].

DNA methylation is a biological process in which methyl groups are added to DNA molecules. Histone modifications include arginine methylation, lysine acetylation, lysine methylation, and serine phosphorylation.

These modifications alter the extent to which DNA wraps around histones and the extent to which genes in DNA can be activated.

Recently, several studies have highlighted the unique role of DNA methylation in aging [ , ]. DNA methylation involves two distinct processes: in DNA, the addition and removal of the 5th methyl group of cytosine 5mC or the 6th methyl group of adenine 6 mA [ ].

In recent years, great progress has been made in several potential methods for estimating biological age, with DNA methylation levels being the most promising [ ]. Studies clearly show that genome-wide DNA methylation levels are associated with chronological age throughout the human lifespan.

Some age-related DNA methylation changes occur in specific regions of the genome and are directional, suggesting the existence of differentially methylated regions associated with age. Thus, biomarkers based on DNA methylation can accurately estimate age, as has been demonstrated by many investigations involving tissues, individuals, and populations [ ].

The reversibility of DNA methylation is the most interesting feature of epigenetic clocks, which suggests that they can be used to measure the effectiveness of anti-aging interventions [ , ]. The link between lifespan and histone methylation has been revealed in a variety of experimental models, including yeast, nematodes, fruit flies, mice and humans [ , ].

To date, the anti-aging and lifespan prolonging effects of HDAC inhibitors have only been investigated in one study of nematodes. The effects of endogenous ketone D-βHB 53 , D-βHB on senescence of nematodes were determined. melanogaster , sodium 4-phenylbutyrate 54 , PBA demonstrated its life-extending potential [ ].

The mean and maximum life span of fruit flies were significantly prolonged by single treatment of sodium butyrate SB Subsequently, other authors confirmed the life-extending ability of D. Melanogaster treated by SB [ , , ].

Trichostatin A 55 , TSA is another HDAC inhibitor with a wide range of epigenetic activity, which was widely used. The phenotypic and epigenetic effects of TSA treatment were very similar to those of SB treatment of D. Increases in mean and maximum lifespan were observed as a result of one-off and continuous TSA treatment [ , ].

In some rodent models, HDAC inhibitors treatment has produced significant anti-aging and healthy lifespan effects, but direct effects on longevity have not been demonstrated. To avoid adverse consequences, the development of stage-specific, tissue-specific, and HDAC specific inhibitors is particularly promising, and considerable research work is currently underway to find such compounds [ ].

MicroRNAs miRNAs are short non-coding RNAs that are involved in post-transcriptional regulation of protein-coding genes. miRNAs regulate lifespan and aging in a variety of organisms. It has been confirmed that Mir regulates the life span of C. miR mutants showed life-prolonging activity, and the overexpression of miR was adequate to reduce the extended lifespan of the mutants [ ].

A highly conserved miRNA miR was significantly up-regulated in Caenorhabditis elegans treated with Astragalus polysaccharides APS. Overexpression of miR induced the extension of nematode lifespan, and vice versa, suggesting that miR regulates nematode lifespan [ ].

miR, miR miR and let-7 were found to be candidate miRNAs involved in the regulation of aging by comparing the miRNA expression of the long-lived fruit flies population fed a low nutrition diet with that of the normal control group fed a high-nutrient diet.

The abundance of miRNAs in the miR family is up-regulated in long-lived daf-2 mutants, suggesting that these miRNAs are effectors of insulin signaling in nematodes.

miR is regulated by the insulin signaling pathway and is partially required for life extension mediated by decreased insulin signaling, dietary restriction, germinal cell ablation, and mild mitochondrial dysfunction.

Daf, isw-1 and ins-1 mRNA were further identified as endogenous targets for miR [ ]. Enoxacin 56 has been reported to extend lifespan by lowering miRp levels, interfering with redox equilibrium and promoting healthy lifespan [ ].

The role of endogenous siRNA in aging has not been studied in comparison with miRNA. By combining nematode sequencing with genomic and genetic approaches, the unprecedented role of endogenous siRNA molecules in protein state maintenance and lifespan extension in reproductive animals is revealed [ ].

The studies performed in animal models have demonstrated that reduced IGF-1 levels or IGF-1 activity can prolong lifespan. In addition, gene polymorphisms of human IGF-1 receptor have been found to relate to exceptional longevity [ ].

A study by Barzilai et al. displayed that low IGF-1 concentrations in plasma anticipated survival in a population of long-lived individuals especially women with a history of cancer [ ].

In dwarf, long-lived mice short of the growth hormone receptor had low IGF-1 levels, were insulin-sensitive, and had a reduced risk of cancer and diabetes despite their obesity [ , , ].

Importantly, similar results have been described in patients with growth hormone receptor-deficient Laron syndrome LS. On this subject, no formal aging research has been conducted in LS patients; however, they are kept from diabetes mellitus and fatal tumors [ , ].

Thus, pharmacological interventions that directly reduce IGF1 levels in adults may improve health and prolong lifespan. Chronic, low-level inflammation is thought to be a main feature of aging.

Many age-related diseases, genes and pathways that modulate inflammation are candidate targets for fighting inflammation [ ]. Despite its importance, the details of the mechanism that triggers the most important stimulus of inflammation remain unknown.

Circulating mitochondrial DNA mtDNA , known as foreign nucleic acid by immune sensors, is a strong inflammatory stimulus that increases with age [ ]. Proinflammatory galactosylated N -glycan is one of the most dominebt biomarkers of human biological age [ ].

Most studies have concentrated on the coding sequences of small portions of the genome. The major parts of res are transposons Tes , which include DNA transposons and retrotransposons, which have the ability to multiply, proliferate, and change genomic positions [ ].

Activation of these specific Tes may lead to genomic and cellular damage, stress, and inflammation leading to senescence [ ]. Analysis of multiple RNA-seq datasets generated from human samples and nematodes revealed that most RE transcripts a increase progressively with age; b can be served to accurately predict age; c may be a good indicator of biological age.

Sestrin 2 is a stress response protein that is primarily regulated by p53 and acts as a cytoprotective agent against genotoxicity and oxidative stress. More importantly, Sestrin 2 is now characterized as a key regulator of cellular metabolism and an effective contributor to cellular homeostasis in disease and normal physiological states.

As inhibitors of mTORC1 and positive regulators of AMPK, sestrins play a protective role in various metabolic diseases such as atherosclerosis, cardiac hypertrophy, cancer, diabetes and obesity. Therefore, sestrins show enormous potential as a therapeutic target and a good prognostic marker for various diseases.

Future research using transgenic animal models will include: conditional, organ-specific knockdown of Sestrin 2 and attempts to link Sestrin 2 levels inpatient biopsy samples to disease progression will help us to identify biochemical pathways regulated by Sestrin 2 in specific diseases.

In addition, the screening and development of small molecule mimics or activators of Sestrin 2 using in vitro and in vivo will help to determine the therapeutic potential of Sestrin 2 as a drug target for various diseases [ ].

Cellular senescence occurs in many types of somatic cells and is a paradigm of counteracting polymorphism. It is a heterogeneous process caused by genetic, epigenetic and environmental factors [ ].

It can be effective at inhibiting damage and carcinogenic signals, thereby improving the reproductive success of young organisms, but it becomes harmful with age, causing tissue response, function and regeneration to deteriorate with age.

Cellular senescence is considered one of the markers of aging. It is believed to contribute to age-related dysfunction, aging and chronic diseases, including AD, atherosclerosis, cancer, chronic obstructive pulmonary disease, diabetes, hepatic steatosis, idiopathic pulmonary fibrosis, myocardial infarction, osteoarthritis, and osteoporosis [ , , ].

Interfering with the pro-aging effects of cell senescence by completely eliminating senescent cells SCs or turning off senescence secretion mechanisms is now being recognized as a potential strategy for treating diseases of aging.

Recently, several transgenic mouse models have been developed that make it possible to visualize, evaluate and destroy senescent cells in vivo. In these models, the promoter of the gene p16INK4A, a protein involved in cell cycle regulation, was used to control cell cycle transcription, inducing the death of senescent cells by using small molecules.

In pMR mouse models, P16INK4A-positive SCs express a viral thymidine kinase that phosphorylates the ganciclovir prodrug, thereby transforming the compound into a toxic metabolite that causes mitochondrial DNA damage and cell death. The p16INK4a promoter can regulate the expression of fluorescent proteins in addition to the death-inducing products of transgenes.

Thus, it is possible to visualize senescent cells in living animals [ ]. Senolytic drugs, used to selectively induce apoptosis in senescent cells, have displayed promise in improving cardiometabolic health indicators and reducing aging-related diseases [ ]. The results of this work suggest that administration of senolytic compounds can improve health and extend lifespan even in old age [ ].

A recent landmark research showed that with the clearance of senescent cells, senolytic therapy was adequate to eliminate Aβ plaques, decrease neuroinflammation, and improve memory in AD model mice [ ].

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