Journal
CELL CYCLE
Volume 6, Issue 13, Pages 1574-1578Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.6.13.4457
Keywords
lifespan; mitochondrial theory of aging; mitochondrial; gene expression; respiration; ROS; TOR; Saccharomyces cerevisiae
Categories
Funding
- NHLBI NIH HHS [HL-059655] Funding Source: Medline
Ask authors/readers for more resources
The Mitochondrial Theory of Aging postulates that accumulation of mtDNA mutations and mitochondrial dysfunction are responsible for generating aging phenotypes and limiting lifespan. Although widely accepted, this theory remains unproven because the evidence supporting it, while substantial, is largely correlative. Furthermore, recent exper imental results in mice with accelerated rates of mtDNA mutagenesis have challenged the traditional formulation of the Mitochondrial Theory, perhaps warranting a reevaluation of some of its core principles. In this perspective, we summarize recent work suggesting that both the quantity and the quality of mitochondrial gene expression play a much greater role in the aging process than previously appreciated. We speculate that this form of mitochondrial dysfunction may operate independently or in concert with mtDNA mutations to promote age - related pathology and limit lifespan.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available