Mitochondrial dysfunction and longevity in animals: Untangling the knot

Mitochondria generate adenosine 5ʹ-triphosphate (ATP) and are a source of potentially toxic reactive oxygen species (ROS). It has been suggested that the gradual mitochondrial dysfunction that is observed to accompany aging could in fact be causal to the aging process. Here we review findings that s...

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Bibliographic Details
Published inScience (American Association for the Advancement of Science) Vol. 350; no. 6265; pp. 1204 - 1207
Main Authors Wang, Ying, Hekimi, Siegfried
Format Journal Article
LanguageEnglish
Published United States American Association for the Advancement of Science 04.12.2015
The American Association for the Advancement of Science
Subjects
Adenosine Triphosphate - metabolism
Adenosines
Aging
Animals
Caenorhabditis elegans Proteins - genetics
Electron Transport - genetics
Electron Transport Complex III - genetics
Knots
Life span
Longevity
Longevity - genetics
Longevity - physiology
Mice
Mice, Knockout
Mitochondria
Mitochondria - genetics
Mitochondria - metabolism
Oxygen
Pathways
Point Mutation
Reactive Oxygen Species - metabolism
REVIEW
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Summary:Mitochondria generate adenosine 5ʹ-triphosphate (ATP) and are a source of potentially toxic reactive oxygen species (ROS). It has been suggested that the gradual mitochondrial dysfunction 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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ISSN:0036-8075
1095-9203
1095-9203
DOI:10.1126/science.aac4357