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Mookerjee, S.A.* ; Divakaruni, A.S.* ; Jastroch, M.* ; Brand, M.D.*

Mitochondrial uncoupling and lifespan.

Mech. Ageing Dev. 131, 463-472 (2010)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
The quest to understand why we age has given rise to numerous lines of investigation that have gradually converged to include metabolic control by mitochondrial activity as a major player. That is, the ideal balance between nutrient uptake, its transduction into usable energy, and the mitigation of damaging byproducts can be regulated by mitochondrial respiration and output (ATP, reactive oxygen species (ROS), and heat). Mitochondrial inefficiency through proton leak, which uncouples substrate oxidation from ADP phosphorylation, can comprise as much as 30% of the basal metabolic rate. This uncoupling is hypothesized to protect cells from conditions that favor ROS production. Uncoupling can also occur through pharmacological induction of proton leak and activity of the uncoupling proteins. Mitochondrial uncoupling is implicated in lifespan extension through its effects on metabolic rate and ROS production. However, evidence to date does not suggest a consistent role for uncoupling in lifespan. The purpose of this review is to discuss recent work examining how mitochondrial uncoupling impacts lifespan.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Sprache englisch
Veröffentlichungsjahr 2010
HGF-Berichtsjahr 0
ISSN (print) / ISBN 0047-6374
e-ISSN 1872-6216
Zeitschrift Mechanisms of Ageing and Development
Quellenangaben Band: 131, Heft: 7-8, Seiten: 463-472 Artikelnummer: , Supplement: ,
Verlag Elsevier
Verlagsort Amsterdam [u.a.]
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Obesity (IDO)
PubMed ID 20363244
DOI 10.1016/j.mad.2010.03.010
WOS ID 000282467300003
Erfassungsdatum 2010-12-31
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