Format

Send to

Choose Destination
See comment in PubMed Commons below
Biochim Biophys Acta. 2011 Apr;1813(4):634-44. doi: 10.1016/j.bbamcr.2011.01.029. Epub 2011 Feb 2.

Mitochondrial longevity pathways.

Author information

1
Division of endocrinology, Endocrine research Unit, The Mayo Clinic, 200 1st Street SW Joseph 5-194, Rochester, MN 55905, USA.

Abstract

Average lifespan has increased over the last centuries, as a consequence of medical and environmental factors, but maximal life span remains unchanged. Better understanding of the underlying mechanisms of aging and determinants of life span will help to reduce age-related morbidity and facilitate healthy aging. Extension of maximal life span is currently possible in animal models with measures such as genetic manipulations and caloric restriction (CR). CR appears to prolong life by reducing oxidative damage. Reactive oxygen species (ROS) have been proposed to cause deleterious effects on DNA, proteins, and lipids, and generation of these highly reactive molecules takes place in the mitochondria. But ROS is positively implicated in cellular stress defense mechanisms and formation of ROS a highly regulated process controlled by a complex network of intracellular signaling pathways. There are endogenous anti-oxidant defense systems that have the potential to partially counteract ROS impact. In this review, we will describe pathways contributing to the regulation of the age-related decline in mitochondrial function and their impact on longevity. This article is part of a Special Issue entitled Mitochondria: the deadly organelle.

PMID:
21295080
PMCID:
PMC3071741
DOI:
10.1016/j.bbamcr.2011.01.029
[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