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Title

Mitochondrial biogenesis and healthy aging

AuthorsLópez-Lluch, Guillermo ; Irusta, Pablo M.; Navas, Plácido ; Cabo, Rafael de
KeywordsAging
Calorie restriction
Mitochondrial biogenesis
PGC-1α
Issue Date9-Jul-2008
PublisherElsevier
CitationExperimental Gerontology 43(9): 813-819 (2008)
AbstractAging is associated with an overall loss of function at the level of the whole organism that has origins in cellular deterioration. Most cellular components, including mitochondria, require continuous recycling and regeneration throughout the lifespan. Mitochondria are particularly susceptive to damage over time as they are the major bioenergetic machinery and source of oxidative stress in cells. Effective control of mitochondrial biogenesis and turnover, therefore, becomes critical for the maintenance of energy production, the prevention of endogenous oxidative stress and the promotion of healthy aging. Multiple endogenous and exogenous factors regulate mitochondrial biogenesis through the peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α). Activators of PGC-1α include nitric oxide, CREB and AMPK. Calorie restriction (CR) and resveratrol, a proposed CR mimetic, also increase mitochondrial biogenesis through activation of PGC-1α. Moderate exercise also mimics CR by inducing mitochondrial biogenesis. Negative regulators of PGC-1α such as RIP140 and 160MBP suppress mitochondrial biogenesis. Another mechanism involved in mitochondrial maintenance is mitochondrial fission/fusion and this process also involves an increasing number of regulatory proteins. Dysfunction of either biogenesis or fission/fusion of mitochondria is associated with diseases of the neuromuscular system and aging, and a greater understanding of the regulation of these processes should help us to ultimately control the aging process.
Description7 páginas, 1 figura.
Publisher version (URL)http://dx.doi.org/10.1016/j.exger.2008.06.014
URIhttp://hdl.handle.net/10261/41182
DOI10.1016/j.exger.2008.06.014
ISSN0531-5565
E-ISSN1873-6815
Appears in Collections:(CABD) Artículos
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