Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
, 25 (1), 57-71

Mammalian Mitochondria and Aging: An Update


Mammalian Mitochondria and Aging: An Update

Timo E S Kauppila et al. Cell Metab.


Mitochondria were first postulated to contribute to aging more than 40 years ago. During the following decades, multiple lines of evidence in model organisms and humans showed that impaired mitochondrial function can contribute to age-associated disease phenotypes and aging. However, in contrast to the original theory favoring oxidative damage as a cause for mtDNA mutations, there are now strong data arguing that most mammalian mtDNA mutations originate as replication errors made by the mtDNA polymerase. Currently, a substantial amount of mitochondrial research is focused on finding ways to either remove or counteract the effects of mtDNA mutations with the hope of extending the human health- and lifespan. This review summarizes the current knowledge regarding the formation of mtDNA mutations and their impact on mitochondrial function. We also critically discuss proposed pathways interlinked with mammalian mtDNA mutations and suggest future research strategies to elucidate the role of mtDNA mutations in aging.

Keywords: ROS; acetylation; aging; biogenesis; mitophagy; mtDNA.

Similar articles

See all similar articles

Cited by 79 PubMed Central articles

See all "Cited by" articles

Publication types

LinkOut - more resources