Journal
BIOLOGICAL CHEMISTRY
Volume 393, Issue 7, Pages 547-564Publisher
WALTER DE GRUYTER GMBH
DOI: 10.1515/hsz-2012-0119
Keywords
autophagy; mitophagy; Nix; Parkin
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Funding
- National Institute of Health (NIH) [R21 AA017421, R01 AA020518-01, R01CA83817]
- National Center for Research Resources [5P20RR021940-07]
- IDeA Networks of Biomedical Research Excellence (INBRE) program of the National Center for Research Resources [P20 RR016475]
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Mitochondria are essential organelles that regulate cellular energy homeostasis and cell death. The removal of damaged mitochondria through autophagy, a process called mitophagy, is thus critical for maintaining proper cellular functions. Indeed, mitophagy has been recently proposed to play critical roles in terminal differentiation of red blood cells, paternal mitochondrial degradation, neurodegenerative diseases, and ischemia or drug-induced tissue injury. Removal of damaged mitochondria through autophagy requires two steps: induction of general autophagy and priming of damaged mitochondria for selective autophagic recognition. Recent progress in mitophagy studies reveals that mitochondrial priming is mediated either by the Pink 1-Parkin signaling pathway or the mitophagic receptors Nix and Bnip3. In this review, we summarize our current knowledge on the mechanisms of mitophagy. We also discuss the pathophysiological roles of mitophagy and current assays used to monitor mitophagy.
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