Format

Send to

Choose Destination
See comment in PubMed Commons below
Mol Cell. 2016 Mar 3;61(5):654-666. doi: 10.1016/j.molcel.2016.01.028.

The Mitochondrial Basis of Aging.

Author information

1
Center for Molecular Medicine, National Heart, Lung and Blood Institute, NIH, Bethesda, MD 20892, USA.
2
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD 20892, USA. Electronic address: richard.youle@nih.gov.
3
Center for Molecular Medicine, National Heart, Lung and Blood Institute, NIH, Bethesda, MD 20892, USA. Electronic address: finkelt@nih.gov.

Abstract

A decline in mitochondrial quality and activity has been associated with normal aging and correlated with the development of a wide range of age-related diseases. Here, we review the evidence that a decline in mitochondria function contributes to aging. In particular, we discuss how mitochondria contribute to specific aspects of the aging process, including cellular senescence, chronic inflammation, and the age-dependent decline in stem cell activity. Signaling pathways regulating the mitochondrial unfolded protein response and mitophagy are also reviewed, with particular emphasis placed on how these pathways might, in turn, regulate longevity. Taken together, these observations suggest that mitochondria influence or regulate a number of key aspects of aging and suggest that strategies directed at improving mitochondrial quality and function might have far-reaching beneficial effects.

PMID:
26942670
PMCID:
PMC4779179
[Available on 2017-03-03]
DOI:
10.1016/j.molcel.2016.01.028
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center