SirT1 inhibition reduces IGF-I/IRS-2/Ras/ERK1/2 signaling and protects neurons
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Sirtuins are known to protect cells and extend life span, but our previous studies indicated that S. cerevisiae Sir2 can also increase stress sensitivity and limit life-span extension. Here we provide evidence for a role of the mammalian Sir2 ortholog SirT1 in the sensitization of neurons to oxidative damage. SirT1 inhibition increased acetylation and decreased phosphorylation of IRS-2; it also reduced activation of the Ras/ERK1/2 pathway, suggesting that SirT1 may enhance IGF-I signaling in part by deacetylating IRS-2. Either the inhibition of SirT1 or of Ras/ERK1/2 was associated with resistance to oxidative damage. Markers of oxidized proteins and lipids were reduced in the brain of old SirT1-deficient mice, but the life span of the homozygote knockout mice was reduced under both normal and calorie-restricted conditions. These results are consistent with findings in S. cerevisiae and other model systems, suggesting that mammalian sirtuins can play both protective and proaging roles.
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SIRT1 has been implicated in promoting oxidative stress through IRS-2/Ras/ERK signaling downstream of insulin/IGF-1 receptors.
“In contrast, SIRT1 has been implicated in promoting oxidative stress through IRS-2/Ras/ERK signaling downstream of insulin/IGF-1 receptors [203].”
From Redox control of senescence and age-related disease. (2017) · cites this paper as [203]
Sirt1 knockout mice show less oxidative stress and more neuroprotection in the ageing brain, yet their lifespan is shortened.
“By contrast, SIRT1 may also have some detrimental effects, as Sirt1 knockout mice show reduced oxidative stress and increased neuroprotection in the ageing brain even though lifespan is shortened (89).”
From Neural mechanisms of ageing and cognitive decline (2010) · cites this paper as [89]
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- Authors
- Li, Y., Xu, W., McBurney, M. W., & Longo, V. D.
- Affiliations
- University of Southern California (US)
- University of Ottawa (CA)
- Corresponding author
- Longo, Valter D.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2008-07
- Volume
- 8
- Issue
- 1
- Pages
- 38-48
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC2822839
- OpenAlex
- W2052764032
- Cited by
- 331
- References
- 70
- Citations by year
- 2026: 4 · 2025: 9 · 2024: 9 · 2023: 10 · 2022: 13 · 2021: 18 · 2020: 16 · 2019: 7 · 2018: 11 · 2017: 15 · 2016: 17 · 2015: 14 · 2014: 20 · 2013: 36 · 2012: 25
- FWCI
- 14.49
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R01AG020642)
- 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
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- SIRT1, sirtuins, Sir2, IGF-1 signaling, insulin receptor substrate 2, oxidative stress, neuroprotection, protein deacetylation, SIRT1 knockout mice, aging, caloric restriction
- MeSH terms
- Animals, Cerebral Cortex, Neurons, Phosphoproteins, Signal Transduction, Receptor, IGF Type 1, Oxidative Stress, ras Proteins, Sirtuins, Intracellular Signaling Peptides and Proteins, Mitogen-Activated Protein Kinase 3, Rats, Insulin Receptor Substrate Proteins, Sirtuin 1
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