Mitochondria and aging: dilution is the solution.
Metabolic component depletion in model systems results in life-span extension, which has been difficult to reconcile with human metabolic pathologies. Recently, Rea et al. (2007) have shown that mitochondrial electron transport chain RNAi phenotypes in the worm C. elegans are dose dependent, providing an alternative view of mitochondrial function in longevity and metabolic diseases.
Molecular and Cell Biology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.
Jenni
J
Durieux
Andrew
A
Dillin
D000375:Aging / Q000378:metabolism*; D000818:Animals; D017173:Caenorhabditis elegans / Q000235:genetics / Q000378:metabolism; D045222:Electron Transport Chain Complex Proteins / Q000037:antagonists & inhibitors / Q000235:genetics; D006801:Humans; D008136:Longevity / Q000235:genetics / Q000502:physiology; D008928:Mitochondria / Q000378:metabolism*; D008954:Models, Biological; D010641:Phenotype; D000091402:Prohibitins; D034622:RNA Interference
D045222:Electron Transport Chain Complex Proteins; C000717331:PHB2 protein, human; D000091402:Prohibitins