Publication Date:
2016-01-20
Description:
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 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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Ying -- Hekimi, Siegfried -- MOP-114891/Canadian Institutes of Health Research/Canada -- MOP-123295/Canadian Institutes of Health Research/Canada -- MOP-97869/Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1204-7. doi: 10.1126/science.aac4357.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, McGill University, Montreal, Quebec H3A 1B1, Canada. ; Department of Biology, McGill University, Montreal, Quebec H3A 1B1, Canada. siegfried.hekimi@mcgill.ca.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785479" target="_blank"〉PubMed〈/a〉
Keywords:
Adenosine Triphosphate/*metabolism
;
Animals
;
Caenorhabditis elegans Proteins/genetics
;
Electron Transport/genetics
;
Electron Transport Complex III/genetics
;
Longevity/genetics/*physiology
;
Mice
;
Mice, Knockout
;
Mitochondria/genetics/*metabolism
;
Point Mutation
;
Reactive Oxygen Species/*metabolism
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
