Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
Volume 1813, Issue 4, Pages 634-644Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbamcr.2011.01.029
Keywords
Mitochondria; Longevity; Lifespan; ROS; Oxidative damage; Caloric restriction
Categories
Funding
- NIH [RO1-AG09531, UL1-RR024150]
- David Murdock-Dole Professorship
- Aarhus University
- Aarhus University Hospital, Denmark
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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. (C) 2011 Elsevier B.V. All rights reserved.
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