Telomere Dysfunction Induces Sirtuin Repression that Drives Telomere-Dependent Disease
Open accessAbstract
Telomere shortening is associated with stem cell decline, fibrotic disorders, and premature aging through mechanisms that are incompletely understood. Here, we show that telomere shortening in livers of telomerase knockout mice leads to a p53-dependent repression of all seven sirtuins. P53 regulates non-mitochondrial sirtuins (Sirt1, 2, 6, and 7) post-transcriptionally through microRNAs (miR-34a, 26a, and 145), while the mitochondrial sirtuins (Sirt3, 4, and 5) are regulated in a peroxisome proliferator-activated receptor gamma co-activator 1 alpha-/beta-dependent manner at the transcriptional level. Administration of the NAD(+) precursor nicotinamide mononucleotide maintains telomere length, dampens the DNA damage response and p53, improves mitochondrial function, and, functionally, rescues liver fibrosis in a partially Sirt1-dependent manner. These studies establish sirtuins as downstream targets of dysfunctional telomeres and suggest that increasing Sirt1 activity alone or in combination with other sirtuins stabilizes telomeres and mitigates telomere-dependent disorders.
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NMN promoted telomere lengthening in aged mice, pre-aging mice, and humans.
“NMN promoted telomere lengthening in aged mice [36], pre-aging mice and humans [37•].”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [36]
The Results (Fig. 6f) report significantly longer telomeres after NMN treatment in G4 mice with dysfunctional telomeres, but not a significant increase in wild-type mice. The Methods describe the mice as 8–16 weeks old, so this does not establish lengthening in aged mice. The sentence assigns the pre-aging-mouse and human claims to a different citation [37•], not this paper. (LLM, conf=0.86)
Experimental — accuracy not yet measuredNMN treatment with 5 mM drinking water for 8 weeks promoted telomere lengthening in G4 mice, dampened the DNA damage response and p53, rescued liver fibrosis, and improved mitochondrial biogenesis and function in a partially SIRT1-dependent manner.
“Treatment with NMN (dissolved in 5-mM drinking water for 8 weeks) promoted telomere lengthening in generation 4 (G4) mice, dampened the DNA damage response and p53, functionally rescued liver fibrosis, and improved the mitochondrial biogenesis and function in a partially SIRT1-dependent manner [36].”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [36]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredIncreased NAD+ levels in liver tissue of NMN-treated G4 mice reversed hyperacetylation of several sirtuin targets, indicating reinforcement of sirtuin activity.
“The increased NAD+ levels in the liver tissue of NMN-treated G4 mice reversed the hyperacetylation of several sirtuin targets indicating the reinforcement of sirtuin activity [36].”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [36]
The concerted action of sirtuins stabilizes telomers and alleviates telomere-associated disorders.
“In addition, the concerted action of sirtuins has been found to stabilize telomers and alleviate telomere-associated disorders (Amano et al. 2019).”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Amano et al. 2019
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- Authors
- Amano, H., Chaudhury, A., Rodriguez-Aguayo, C., Lu, L., Akhanov, V., Catic, A., Popov, Y. V., Verdin, E., Johnson, H., Stossi, F., Sinclair, D. A., Nakamaru-Ogiso, E., Lopez-Berestein, G., Chang, J. T., Neilson, J. R., Meeker, A., Finegold, M., Baur, J. A., & Sahin, E.
- Affiliations
- Baylor College of Medicine (US)
- Philips (United States) (US)
- Beth Israel Deaconess Medical Center (US)
- Gladstone Institutes (US)
- Harvard University (US)
- The University of Texas Health Science Center at Houston (US)
- Johns Hopkins University (US)
- University of Pennsylvania (US)
- ORCID
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2019-06
- Volume
- 29
- Issue
- 6
- Pages
- 1274-1290.e9
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC6657508
- OpenAlex
- W2927492624
- Cited by
- 182
- References
- 51
- Citations by year
- 2026: 13 · 2025: 31 · 2024: 27 · 2023: 34 · 2022: 26 · 2021: 22 · 2020: 20 · 2019: 9
- FWCI
- 10.14
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (AG043483, DK098656, CA125123, DK56338, FP00000019, R01DK115454)
- National Institute on Aging (R01AG047924)
- National Cancer Institute (CA190467)
- American Cancer Society (RSG-15-088-01RMC)
- Glenn Foundation for Medical Research (R01 DK100263, AG043483, R21 DE027490, R01 AG019719, DK098656, R37 AG028730)
- Cancer Prevention and Research Institute of Texas (RP170719, RP150578)
- Topics
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- telomere shortening, sirtuins, p53, liver fibrosis, microRNA, miR-34a, miR-26a, miR-145, SIRT1, nicotinamide mononucleotide, NAD+ precursors, DNA damage response, mitochondrial function, premature aging
- MeSH terms
- Animals, Cells, Cultured, Embryo, Mammalian, Female, Humans, Liver, Liver Cirrhosis, Male, Mice, Inbred C57BL, Mitochondria, Liver, Nicotinamide Mononucleotide, Down-Regulation, Gene Expression Regulation, Enzymologic, Mice, Knockout, Telomerase, Sirtuins, Mice, Sirtuin 1, HEK293 Cells, Telomere Homeostasis, Telomere Shortening
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