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Mitochondrial Quality Control: Role in Cardiac Models of Lethal Ischemia-Reperfusion Injury

1
Cardiovascular Research Institute, Wayne State University School of Medicine, Detroit, MI 48201, USA
2
Department of Biochemistry, Microbiology and Immunology, Wayne State University School of Medicine, Detroit, MI 48201, USA
3
Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201, USA
4
Departments of Emergency Medicine and Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48109, USA
5
Department of Emergency Medicine, Wayne State University School of Medicine, Detroit, MI 48201, USA
*
Author to whom correspondence should be addressed.
Cells 2020, 9(1), 214; https://doi.org/10.3390/cells9010214
Received: 11 December 2019 / Revised: 10 January 2020 / Accepted: 12 January 2020 / Published: 15 January 2020
(This article belongs to the Special Issue Mitochondrial Dynamics: Fusion and Fission)
The current standard of care for acute myocardial infarction or ‘heart attack’ is timely restoration of blood flow to the ischemic region of the heart. While reperfusion is essential for the salvage of ischemic myocardium, re-introduction of blood flow paradoxically kills (rather than rescues) a population of previously ischemic cardiomyocytes—a phenomenon referred to as ‘lethal myocardial ischemia-reperfusion (IR) injury’. There is long-standing and exhaustive evidence that mitochondria are at the nexus of lethal IR injury. However, during the past decade, the paradigm of mitochondria as mediators of IR-induced cardiomyocyte death has been expanded to include the highly orchestrated process of mitochondrial quality control. Our aims in this review are to: (1) briefly summarize the current understanding of the pathogenesis of IR injury, and (2) incorporating landmark data from a broad spectrum of models (including immortalized cells, primary cardiomyocytes and intact hearts), provide a critical discussion of the emerging concept that mitochondrial dynamics and mitophagy (the components of mitochondrial quality control) may contribute to the pathogenesis of cardiomyocyte death in the setting of ischemia-reperfusion.
Keywords: heart; ischemia; reperfusion; mitochondria; fission; fusion; mitophagy heart; ischemia; reperfusion; mitochondria; fission; fusion; mitophagy
MDPI and ACS Style

Kulek, A.R.; Anzell, A.; Wider, J.M.; Sanderson, T.H.; Przyklenk, K. Mitochondrial Quality Control: Role in Cardiac Models of Lethal Ischemia-Reperfusion Injury. Cells 2020, 9, 214.

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