Journal
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
Volume 95, Issue -, Pages 42-49Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2015.11.023
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Funding
- NHLBI NIH HHS [R01 HL128441, R01 HL059888, R01 HL128071] Funding Source: Medline
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Mitochondria can undergo autophagic elimination for differing reasons, e.g. as part of a cell-wide macroautophagic response, as part of mitochondrial turnover during metabolic remodeling, or in the case of selective mitophagic destruction of dysfunctional mitochondria, during mitochondrial quality control. Multiple mechanistically distinct pathways converge upon, and activate, mitochondrial autophagy. Here, the evidence supporting a role for the prototypical mitochondrial quality control pathway, PINK1-Parkin mediated mitophagy, in cardiac homeostasis and heart disease is reviewed. Contrary to popular wisdom based on findings from non cardiac systems, current data do not support a major role for Parkin-mediated mitophagy as a mechanism for constitutive mitochondrial housekeeping, and instead suggest that this pathway primarily functions in adult hearts as an inducible cardiac stress-response mechanism. Recent findings have also uncovered an unsuspected role for Parkin-mediated mitochondria] turnover in the normal perinatal transformation of myocardial metabolism. (C) 2015 Elsevier Ltd. All rights reserved.
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