Journal
CARDIOVASCULAR RESEARCH
Volume 94, Issue 2, Pages 190-196Publisher
OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvr312
Keywords
Mitochondria; Fission; Fusion; Autophagy; Myocytes
Categories
Funding
- NIH [R01HL087023, R01HL101217, R01HL092136]
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available