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Mammalian Sirtuins: Biological Insights and Disease Relevance
Open accessAbstract
Aging is accompanied by a decline in the healthy function of multiple organ systems, leading to increased incidence and mortality from diseases such as type II diabetes mellitus, neurodegenerative diseases, cancer, and cardiovascular disease. Historically, researchers have focused on investigating individual pathways in isolated organs as a strategy to identify the root cause of a disease, with hopes of designing better drugs. Studies of aging in yeast led to the discovery of a family of conserved enzymes known as the sirtuins, which affect multiple pathways that increase the life span and the overall health of organisms. Since the discovery of the first known mammalian sirtuin, SIRT1, 10 years ago, there have been major advances in our understanding of the enzymology of sirtuins, their regulation, and their ability to broadly improve mammalian physiology and health span. This review summarizes and discusses the advances of the past decade and the challenges that will confront the field in the coming years.
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“Proposed drivers of physiological aging include the accumulation of DNA damage, increased ROS production, telomere shortening, cellular senescence, and defects in nuclear envelope architecture (Bernardes de Jesus and Blasco, 2013;Guarente, 2008;Haigis and Sinclair, 2009;Kennedy and Lamming, 2016;Soultoukis and Partridge, 2016;Steffen and Dillin, 2016).”
From In Vivo Amelioration of Age-Associated Hallmarks by Partial Reprogramming. (2016) · cites this paper as Haigis and Sinclair, 2009
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“Sirtuins are NAD+‐dependent enzymes implicated in a range of physiological and pathophysiological conditions, including AS, diabetes mellitus, cancer, longevity, and neurodegeneration, through deacetylation of numerous substrates.42”
From Trimethylamine‐N‐Oxide Induces Vascular Inflammation by Activating the NLRP3 Inflammasome Through the SIRT3‐SOD2‐mtROS Signaling Pathway (2017) · cites this paper as [42]
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Metadata
- Authors
- Haigis, M. C., & Sinclair, D. A.
- Affiliations
- Harvard University (US)
- Venue
- Annual Review of Pathology: Mechanisms of Disease
- Publisher
- Annual Reviews
- Published
- 2010-01-01
- Volume
- 5
- Issue
- 1
- Pages
- 253-295
- ISSN
- 1553-4006 (ISSN-L)
- 1553-4014
- PMC
- PMC2866163
- OpenAlex
- W2118964113
- Cited by
- 2,085
- References
- 56
- Citations by year
- 2026: 78 · 2025: 118 · 2024: 80 · 2023: 113 · 2022: 123 · 2021: 152 · 2020: 143 · 2019: 124 · 2018: 148 · 2017: 115 · 2016: 142 · 2015: 117 · 2014: 154 · 2013: 145 · 2012: 149
- FWCI
- 13.23
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annual Review of Pathology Mechanisms of Disease (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R01AG032375, P01AG027916, R01AG028730, R01AG019719)
- 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 › Molecular Biology › Nuclear Receptors and Signaling
- Keywords
- sirtuins, SIRT1, aging, healthspan, longevity, type 2 diabetes, neurodegenerative diseases, cancer, cardiovascular disease
- MeSH terms
- Aging, Animals, Cardiovascular Diseases, Humans, Longevity, Metabolic Diseases, Neoplasms, Neurodegenerative Diseases, Sirtuins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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