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NAD + repletion improves mitochondrial and stem cell function and enhances life span in mice
Open accessAbstract
A dietary supplement protects aging muscle: The oxidized form of cellular nicotinamide adenine dinucleotide (NAD + ) is critical for mitochondrial function, and its supplementation can lead to increased longevity. Zhang et al. found that feeding the NAD + precursor nicotinamide riboside (NR) to aging mice protected them from muscle degeneration (see the Perspective by Guarente). NR treatment enhanced muscle function and also protected mice from the loss of muscle stem cells. The treatment was similarly protective of neural and melanocyte stem cells, which may have contributed to the extended life span of the NR-treated animals. Science , this issue p. 1436 ; see also p. 1396
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“Mounting evidence supports a critical role for NAD+ in stem cell rejuvenation, including in HSCs, endothelial stem cells, muscle stem cells, and melanocyte stem cells (Das et al., 2018; Vannini et al., 2019; Zhang et al., 2016).”
From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Zhang et al., 2016
In the citing paper
“Similarly, NR treatment of aged mice resulted in increased proliferation and increased neurogenesis in both the subventricular zone and the dentate gyrus of the hippocampus in aged mice (Zhang et al., 2016).”
From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Zhang et al., 2016
In the citing paper
“In primary cell culture, supplementation with NR delays cellular senescence (Wiley et al., 2016), and NR treatment also reduces the senescent state in both NSCs and other stem cell types (Zhang et al., 2016).”
From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Zhang et al., 2016
In the citing paper
“NR supplementation delayed senescence of adult NSCs in 2-year-old mice (Zhang et al., 2016), suggesting a role for a deficit in NAD+ or one or more of the enzymes it supports in neural-cell senescence.”
From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Zhang et al., 2016
In the citing paper
“NR administration in old mice showed a small but significant increase in lifespan (5%)198.”
From NAD+ metabolism and its roles in cellular processes during ageing (2021) · cites this paper as [198]
In the citing paper
“Treatment with NR also improved muscle stem cell functions by regulating mitochondrial metabolism in a mouse model of muscular dystrophy197,198.”
From NAD+ metabolism and its roles in cellular processes during ageing (2021) · cites this paper as [198]
In the citing paper
“In mice, NR causes a wide range of beneficial effects, including a moderate lifespan extension [202].”
From Immunosenescence: a key player in cancer development (2020) · cites this paper as [202]
In the citing paper
“Additionally, nicotinamide riboside treatment in aging mice increased skeletal muscle function by preventing stem cell senescence, improved mitochondrial function, and a higher expression of genes involved in the TCA cycle and OXPHOS (266).”
From Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease (2018) · cites this paper as [266]
In the citing paper
“Reduced NAD+ levels in skeletal muscle of aged or Nampt deficient mice alter mitochondrial bioenergetics and impair muscle mass, strength and endurance49,50,52,53”
From Mitochondrial oxidative capacity and NAD+ biosynthesis are reduced in human sarcopenia across ethnicities (2019) · cites this paper as [53]
In the citing paper
“the conversion of these precursors to NAD+ bypasses the rate limited enzyme NAMPT”
From Mitochondrial oxidative capacity and NAD+ biosynthesis are reduced in human sarcopenia across ethnicities (2019) · cites this paper as [53]
In the citing paper
“new therapeutic strategies have emerged to restore NAD+ levels in muscle by administration of dietary NAD+ precursors such as NR or NMN46,53,54”
From Mitochondrial oxidative capacity and NAD+ biosynthesis are reduced in human sarcopenia across ethnicities (2019) · cites this paper as [53]
In the citing paper
“For example, some old MuSCs become senescent, a state characterized by irreversible cell cycle arrest and secretion of cytokines and other proteins (senescence-associated secreted phenotype)39–43.”
From Ageing and rejuvenation of tissue stem cells and their niches (2023) · cites this paper as [39]
In the citing paper
“NAD precursors such as nicotinamide riboside can restore ageing defects in ISCs120, as well as in MuSCs, NSCs and melanocyte stem cells39.”
From Ageing and rejuvenation of tissue stem cells and their niches (2023) · cites this paper as [39]
In the citing paper
“The administration of NAD precursors, in particular nicotinamide riboside and nicotinamide mononucleotide, has shown benefits in terms of healthspan219 and lifespan39.”
From Ageing and rejuvenation of tissue stem cells and their niches (2023) · cites this paper as [39]
In the citing paper
“Nicotinamide riboside also has a beneficial effects on old MuSCs, NSCs and melanocyte stem cells, in part by rescuing mitochondrial function39.”
From Ageing and rejuvenation of tissue stem cells and their niches (2023) · cites this paper as [39]
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Giblin, W., & Lombard, D. B. (2015) · Elsevier eBooks · doi:10.1016/b978-0-12-411596-5.00003-4 · Cited by 12
Pawlikowski, B. T., Betta, N. D., Antwine, T., & Olwin, B. B. (2019) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/627851 · Cited by 13
“…in aged mice Skeletal muscle in aged mammals loses function, is reduced in mass, possess smaller myofibers and reduced numbers of MuSCs (Brack et al., 2005; Chakkalakal et al., 2012; Collins et al., 2007; Gibson & Schultz, 1983; Shefer et al., 2006; Sousa-Victor et al., 2014; Zhang et al., 2016).”
BackgroundResultInfluentialNowacka, A., Śniegocki, M., Śniegocka, M., & Ziółkowska, E. (2025) · Antioxidants · doi:10.3390/antiox14080911 · Cited by 11
Kang, S., Park, J.-W., Cho, E., Kim, D., Ye, S., Jeong, E. T., Jun, S., & Kang, N. G. (2025) · Biomedicines · doi:10.3390/biomedicines13102395 · Cited by 13
“A decline in NAD + is a noticeable hallmark of aging, and its supplementation can ameliorate aging-related metabolic conditions and even extend the lifespan of living organisms [5–10].”
Chen, Y., Liang, Y., Shen, J., Wang, Y., Qiu, B., Hou, H., & Qiu, X. (2025) · Research · doi:10.34133/research.0973 · Cited by 11
“Numerous studies have shown that whether under in vitro hypoxia/reoxygenation conditions or in vivo ischemia/reperfusion injury, NAD + levels consistently decrease: At the same time, NADH accumulates, contributing to both cardiomyocyte dysfunction and senescence of transplanted ADSCs [ 16 , 17 ].”
Metcalfe, M., David, B. T., Langley, B. C., & Hill, C. E. (2023) · Experimental Neurology · doi:10.1016/j.expneurol.2023.114479 · Cited by 11
Changes in the Mitochondria in the Aging Process—Can α-Tocopherol Affect Them?
Napolitano, G., Fasciolo, G., Tomajoli, M. T. M., & Venditti, P. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241512453 · Cited by 12
Premature senescence and cardiovascular disease following cancer treatments: mechanistic insights
Jain, A., Casanova, D., Padilla, A. V., Paniagua-Bojorges, A., Kotla, S., Ko, K. A., Samanthapudi, V. S. K., Chau, K. M., Nguyen, M. T., Wen, J. J., et al. (2023) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2023.1212174 · Cited by 11
Label-free metabolic optical biomarkers track stem cell fate transition in real time
Zhou, H., Li, I. A., Bramlett, C. S., Wang, B., Hao, J., Yen, D. P., Ando, Y., Fraser, S. E., Lu, R., & Shen, K. (2024) · Science Advances · doi:10.1126/sciadv.adi6770 · Cited by 11
Vitamin A retinoic acid contributes to muscle stem cell and mitochondrial function loss in old age
Fraczek, P. M., Duran, P., Yang, B. A., Ferre, V., Alawieh, L., Castor‐Macias, J. A., Wong, V. T., Guzman, S. D., Piotto, C., Itsani, K., et al. (2025) · JCI Insight · doi:10.1172/jci.insight.183706 · Cited by 12
“These results show that the pathological degeneration of MuSCs in old age, which is linked to dysfunctional mitochondria and oxidative damage, can be partially alleviated by targeting RA signaling (41).”
Mitochondrial and microtubule defects in Exfoliation Glaucoma
Venkatesan, A., Ridilla, M., Castro, N., Wolosin, J. M., Henty-Ridilla, J. L., Knox, B. E., Ganapathy, P. S., Brown, J. S., DeVincentis, A. F., Sieminski, S. F., et al. (2025) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2025.03.046 · Cited by 11
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Changing ROS, NAD and AMP: A path to longevity via mitochondrial therapeutics
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“The past decades have provided evidence that raising NAD levels by supplementation of niacin precursors to cells, tissues, or entire organisms can rejuvenate and even extend life-span.(34) Platelets are no different and respond to NR supplementation by increasing intracellular NAD levels.”
BackgroundCombinatorial metabolism drives the naive to primed pluripotent chromatin landscape
Ehnes, D. D., Hussein, A. M., Ware, C. B., Mathieu, J., & Ruohola‐Baker, H. (2020) · Experimental Cell Research · doi:10.1016/j.yexcr.2020.111913 · Cited by 12
Herpetosiphon Secondary Metabolites Inhibit Amyloid-β Toxicity in Human Primary Astrocytes
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The Discovery of Druggable Anti-aging Agents
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“Indeed, 10–12 weeks of NR supplementation improved dystrophic muscle function and enhanced satellite cell and mitochondrial function (Ryu et al., 2016; Zhang et al., 2016).”
BackgroundMethodDNA Methylation Ageing Atlas Across 17 Human TissuesPreprint
Jacques, M., Seale, K., Voisin, S. A. C., Lysenko, A., Grolaux, R., Jones, B., Lamon, S., Levinger, I., Bauer, C., Sharples, A. P., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.07.21.665830 · Cited by 12
Sun, X., Su, L., Bu, T., & Zhang, Y. (2023) · Frontiers in Public Health · doi:10.3389/fpubh.2023.1287421 · Cited by 10
Mitochondrial Dynamics in Aging Heart
Patyal, P., Azhar, G., Verma, A., Sharma, S., Shrivastava, J., Abdi, S. A. H., Zhang, X., & Wei, J. Y. (2025) · Biomedicines · doi:10.3390/biomedicines13112603 · Cited by 14
“NAD + precursors like nicotinamide riboside (NR) also induce mitophagy via induction of sirtuin-1 (SIRT1) and PGC-1 α pathways [143].”
Importance of Nutrient Availability and Metabolism for Skeletal Muscle Regeneration
Blum, J., Epstein, R., Watts, S. A., & Thalacker‐Mercer, A. E. (2021) · Frontiers in Physiology · doi:10.3389/fphys.2021.696018 · Cited by 15
“Succinylation of lysine residues impacts proteins involved in FAO, branched chain amino acid catabolism, ketone body synthesis, the pentose phosphate pathway, and the TCA cycle (Rardin et al., 2013; Zhang et al., 2015; Zhou et al., 2016).”
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Self-citationBiological Functions and Therapeutic Potential of NAD+ Metabolism in Gynecological Cancers
Myong, S., Nguyen, A. Q., & Challa, S. (2024) · Cancers · doi:10.3390/cancers16173085 · Cited by 10
“Sirtuins are NAD + -dependent deacetylase enzymes that are also responsible for cleaving NAD + to produce NAM and transfer acetyl groups from the lysine residues on a target protein onto an ADP-ribose molecule [42].”
BackgroundTauroursodeoxycholic acid targets HSP90 to promote protein homeostasis and extends healthy lifespan
Liu, J., Wang, Y., Guo, Y., Zheng, R.-Q., Wang, Y., Shen, Y., Liu, Y., Cao, A.-P., Wang, R., Xie, B.-Y., et al. (2024) · Science China Life Sciences · doi:10.1007/s11427-024-2717-6 · Cited by 13
“…precursors to Nicotinamide adenine dinucleotide (NAD), including NR, NMN, and NAM, have been shown to promote longevity in worms, prolong the lifespan of mice, or improve their health status in old age (Mills et al., 2016; Mitchell et al., 2018; Mouchiroud et al., 2013; Zhang et al., 2016).”
Advancements in NADH Oxidase Nanozymes: Bridging Nanotechnology and Biomedical Applications
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Prognostic value of tryptophan catabolism-base scores in acute myocardial infarction patients
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“There have been a few studies of NAD + boosters in treating CVD or metabolic diseases [33,34].”
Cardiac Damage in Hypertension: From Molecular Mechanisms to Novel Therapeutic Approaches
Gallo, G., & Rubattu, S. D. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26125610 · Cited by 12
Nanomaterials intervene in cell senescence to reinforce cancer therapy
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Metadata
- Authors
- Zhang, H., Ryu, D., Wu, Y., Gariani, K., Wang, X., Luan, P., D’Amico, D., Ropelle, E. R., Lutolf, M. P., Aebersold, R., Schoonjans, K., Menzies, K. J., & Auwerx, J.
- Affiliations
- École Polytechnique Fédérale de Lausanne (CH)
- ETH Zurich (CH)
- Laboratory of Integrative and Systems Physiology, École Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland.
- Universidade Estadual de Campinas (UNICAMP) (BR)
- Laboratory of Stem Cell Bioengineering, EPFL, 1015 Lausanne, Switzerland.
- University of Zurich (CH)
- University of Ottawa (CA)
- Corresponding author
- Menzies, Keir J.
- Auwerx, Johan
- ORCID
- Venue
- Science
- Published
- 2016-06-17
- Volume
- 352
- Issue
- 6292
- Pages
- 1436-1443
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2343193821
- Cited by
- 1,255
- References
- 54
- Citations by year
- 2026: 109 · 2025: 139 · 2024: 110 · 2023: 123 · 2022: 142 · 2021: 151 · 2020: 131 · 2019: 111 · 2018: 114 · 2017: 93 · 2016: 29
- FWCI
- 66.83
- Type
- journal article
- Language
- en
- Open access
- green
- infoscience.epfl.ch
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Archive ouverte UNIGE (University of Geneva) (publishedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
- Funders
- University of Ottawa
- Heart and Stroke Foundation of Canada
- NIH (R01AG043930)
- Krebsforschung Schweiz/SwissCancerLeague (KFS-3082-02-2013)
- Systems X (SySX.ch 2013/153)
- Swiss National Science Foundation (31003A-140780)
- Topics
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Keywords
- nicotinamide riboside, muscle stem cells, mitochondrial unfolded protein response, prohibitin, mitochondrial function, aging, lifespan extension, neural stem cells, melanocyte stem cells, mdx mice, muscular dystrophy, cellular reprogramming
- MeSH terms
- Prohibitins, Animals, Disease Models, Animal, Longevity, Melanocytes, Mice, Inbred C57BL, Mitochondria, Muscular Dystrophies, NAD, Niacinamide, Pyridinium Compounds, Repressor Proteins, Cellular Senescence, Mice, Inbred mdx, Oxidative Stress, Myoblasts, Skeletal, Mice, Unfolded Protein Response, Neural Stem Cells, Cellular Reprogramming
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