Mitochondrial signaling, TOR, and life span
Abstract
Growing evidence supports the concept that mitochondrial metabolism and reactive oxygen species (ROS) play a major role in aging and determination of an organism's life span. Cellular signaling pathways regulating mitochondrial activity, and hence the generation of ROS and retrograde signaling events originating in mitochondria, have recently moved into the spotlight in aging research. Involvement of the energy-sensing TOR pathway in both mitochondrial signaling and determination of life span has been shown in several studies. This brief review summarizes the recent progress on how mitochondrial signaling might contribute to the aging process with a particular emphasis on TOR signaling from invertebrates to humans.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Reduced TOR signalling has been shown to extend lifespan in yeast, worms and flies.
“Reduced TOR signalling has been shown to extend lifespan in yeast, worms and flies (reviewed in ref. 57).”
From Neural mechanisms of ageing and cognitive decline (2010) · cites this paper as [57]
The signalling pathway of the kinase TOR is a central regulator of protein homeostasis that acts to inhibit autophagy and messenger RNA translation.
“The signalling pathway of the kinase TOR is a central regulator of protein homeostasis that acts to inhibit autophagy and messenger RNA translation.”
From Neural mechanisms of ageing and cognitive decline (2010) · cites this paper as [57]
The citation lists haven’t been fetched yet
References 45 · Cited by 106
- Authors
- Schieke, S. M., & Finkel, T.
- Affiliations
- National Institutes of Health (US)
- Venue
- Biological Chemistry
- Publisher
- Walter de Gruyter GmbH
- Published
- 2006-01-01
- Volume
- 387
- Issue
- 10/11
- Pages
- 1357-61
- ISSN
- 1431-6730 (ISSN-L)
- 1437-4315
- OpenAlex
- W1985629790
- Cited by
- 106
- References
- 45
- Citations by year
- 2025: 2 · 2024: 3 · 2023: 4 · 2022: 1 · 2021: 2 · 2020: 5 · 2019: 4 · 2018: 2 · 2016: 1 · 2015: 3 · 2014: 6 · 2013: 8 · 2012: 12
- FWCI
- 0.86
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biological Chemistry (publishedVersion)
- PubMed (publishedVersion)
- 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
- mitochondrial signaling, TOR signaling, lifespan, aging, reactive oxygen species, mitochondrial metabolism, retrograde signaling, energy sensing, invertebrates, human
- MeSH terms
- Aging, Animals, Humans, Life Expectancy, Mitochondria, Protein Kinases, Signal Transduction, 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 ›
Are you an author, or do you see a problem with this page? Request a review
