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New roles for mitochondria in cell death in the reperfused myocardium.

Authors
Type
Published Article
Journal
Cardiovascular Research
1755-3245
Publisher
Oxford University Press
Publication Date
Volume
94
Issue
2
Pages
190–196
Identifiers
DOI: 10.1093/cvr/cvr312
PMID: 22108916
Source
Medline
License
Unknown

Abstract

Mitochondria play an important role in regulating the life and death of cells. They provide the cell with energy via oxidative phosphorylation but can quickly turn into death-promoting organelles in response to stress by disrupting adenosine triphosphate synthesis, releasing pro-death proteins, and producing reactive oxygen species. Due to their high-energy requirement, cardiac myocytes are abundant in mitochondria and as a result, particularly vulnerable to mitochondrial defects. Myocardial ischaemia and reperfusion are associated with mitochondrial dysfunction and cell death. Therefore, future therapies will focus on preserving mitochondrial integrity and function in hopes of minimizing the impact of ischaemia/reperfusion (I/R) injury. It is well established that myocardial I/R activates both necrosis and apoptosis, and that blocking either process reduces the levels of injury. However, recent studies have demonstrated that alterations in mitochondrial dynamics or clearance of mitochondria via autophagy also can contribute to cell death in the myocardium. In this review, we will discuss these new developments and their impact on the role of cardiac mitochondria in cell death following reperfusion in the heart.

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