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Mitochondrial dysfunction and longevity in animals: Untangling the knot

Ying Wang, Siegfried Hekimi

Science · 2015 · ▲ 257 citations

Abstract

Mitochondria generate adenosine 5'-triphosphate (ATP) and are a source of potentially toxic reactive oxygen species (ROS). It has been suggested that the gradual mitochondrial dysfunction(definition) that is observed to accompany aging could in fact be causal to the aging process. Here we review findings that suggest that age-dependent mitochondrial dysfunction is not sufficient to limit life span. Furthermore, mitochondrial ROS are not always deleterious and can even stimulate pro-longevity pathways. Thus, mitochondrial dysfunction plays a complex role in regulating longevity.

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Provenance

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OpenAlex
DOI
10.1126/science.aac4357
Canonical
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2026-06-22 MST

Cite this

APA
Wang, Y., &amp; Hekimi, S. (2015). Mitochondrial dysfunction and longevity in animals: Untangling the knot. <em>Science</em>. https://doi.org/10.1126/science.aac4357
Vancouver
Wang Y, Hekimi S. Mitochondrial dysfunction and longevity in animals: Untangling the knot. Science. 2015. doi:10.1126/science.aac4357.
BibTeX
@unpublished{ying2015Mitoch, title = {Mitochondrial dysfunction and longevity in animals: Untangling the knot}, author = {Ying Wang and Siegfried Hekimi}, journal = {Science}, year = {2015}, doi = {10.1126/science.aac4357}, }

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