The role of mitochondria in mTOR‐regulated longevity
Open accessAbstract
Several unbiased genome-wide RNA interference (RNAi) screens have pointed to mitochondrial metabolism as the major factor for lifespan regulation. However, conflicting data remain to be clarified concerning the mitochondrial free radical theory of aging (MFRTA). Recently, mTOR (mechanistic target of rapamycin) has been proposed to be the central regulator of aging although how mTOR modulates lifespan is poorly understood. Interestingly, mTOR has been shown to regulate many aspects of mitochondrial function, such as mitochondrial biogenesis, apoptosis, mitophagy and mitochondrial hormesis (mitohormesis) including the retrograde response and mitochondrial unfolded protein response (mito-UPR). Here we discuss the data linking mitochondrial metabolism to mTOR regulation of lifespan, suggesting that hormetic effects may be key to explaining some controversial results regarding the MFRTA. We also discuss the possibility that dysfunction of mitochondrial adaptive responses rather than free radicals per se contributes to the aging process.
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Rapamycin prolongs lifespan by inhibiting the effects of mTOR.
“Rapamycin prolongs lifespan by inhibiting the effects of mTOR.”
From Metformin, the Aspirin of the 21st Century: Its Role in Gestational Diabetes Mellitus, Prevention of Preeclampsia and Cancer, and the Promotion of Longevity (2017) · cites this paper as [239]
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Romero, R., Erez, O., Hüttemann, M., Maymon, E., Panaitescu, B., Conde-Agudelo, A., Pacora, P., Yoon, B. H., & Grossman, L. I. (2017) · American Journal of Obstetrics and Gynecology · doi:10.1016/j.ajog.2017.06.003 · Cited by 253 · see citing works
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Non‐mammalian Hosts and Photobiomodulation: Do All Life‐forms Respond to Light?
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- Authors
- Wei, Y., Zhang, Y., Cai, Y., & Xu, M.
- Affiliations
- Shanghai Jiao Tong University (CN)
- No.3 People's Hospital School of Medicine, Shanghai Jiao Tong University 280 Mohe Road Shanghai 201900 China
- Corresponding author
- Wei, Yuehua
- ORCID
- Venue
- Biological Reviews
- Publisher
- Wiley
- Published
- 2014-03-28
- Volume
- 90
- Issue
- 1
- Pages
- 167-181
- ISSN
- 0006-3231 (ISSN-L)
- 1464-7931
- 1469-185X
- OpenAlex
- W1525028956
- Cited by
- 56
- References
- 195
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 2 · 2023: 12 · 2022: 6 · 2021: 4 · 2020: 4 · 2019: 5 · 2018: 4 · 2017: 5 · 2016: 2 · 2015: 5 · 2014: 1
- FWCI
- 0.49
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Biological reviews/Biological reviews of the Cambridge Philosophical Society (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81200248)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- mTOR, longevity, lifespan regulation, mitochondrial metabolism, mitochondrial biogenesis, mitophagy, mitochondrial unfolded protein response, retrograde response, apoptosis, aging
- MeSH terms
- Animals, Gene Expression Regulation, Longevity, Mitochondria, TOR Serine-Threonine Kinases
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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