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Biochim Biophys Acta. 2011 Jul;1813(7):1295-301. doi: 10.1016/j.bbamcr.2010.11.017. Epub 2010 Dec 13.

Mitochondrial turnover in the heart.

Author information

1
BioScience Center, San Diego State University, 5500 Campanile Drive, San Diego, CA 92182-4650, USA. robbieg@sciences.sdsu.edu

Abstract

Mitochondrial quality control is increasingly recognized as an essential element in maintaining optimally functioning tissues. Mitochondrial quality control depends upon a balance between biogenesis and autophagic destruction. Mitochondrial dynamics (fusion and fission) allows for the redistribution of mitochondrial components. We speculate that this permits sorting of highly functional components into one end of a mitochondrion, while damaged components are segregated at the other end, to be jettisoned by asymmetric fission followed by selective mitophagy. Ischemic preconditioning requires autophagy/mitophagy, resulting in selective elimination of damaged mitochondria, leaving behind a population of robust mitochondria with a higher threshold for opening of the mitochondrial permeability transition pore. In this review we will consider the factors that regulate mitochondrial biogenesis and destruction, the machinery involved in both processes, and the biomedical consequences associated with altered mitochondrial turnover. This article is part of a Special Issue entitled: Mitochondria and Cardioprotection.

PMID:
21147177
PMCID:
PMC3335292
DOI:
10.1016/j.bbamcr.2010.11.017
[Indexed for MEDLINE]
Free PMC Article

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