Mitochondrial dysfunction and longevity in animals: Untangling the knot
Author(s) -
Ying Wang,
Siegfried Hekimi
Publication year - 2015
Publication title -
science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 12.556
H-Index - 1186
eISSN - 1095-9203
pISSN - 0036-8075
DOI - 10.1126/science.aac4357
Subject(s) - longevity , mitochondrion , adenosine triphosphate , reactive oxygen species , life span , biology , mitochondrial dna , microbiology and biotechnology , genetics , biochemistry , evolutionary biology , gene
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.
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