Mitochondrial function: The heart of myocardial preservation

被引:21
作者
McFalls, EO
Liem, D
Schoonderwoerd, K
Lamers, J
Sluiter, W
Duncker, D
机构
[1] Univ Minnesota, Vet Affairs Med Ctr, Dept Med, Minneapolis, MN 55417 USA
[2] Erasmus MC, Dept Expt Cardiol & Biochem, Rotterdam, Netherlands
来源
JOURNAL OF LABORATORY AND CLINICAL MEDICINE | 2003年 / 142卷 / 03期
关键词
D O I
10.1016/S0022-2143(03)00109-4
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Over the past several decades, it has become widely recognized that the mitochondria serve an important role in energy production and transfer to myocardial cells. More recently, mitochondria have been shown to play a key role in cell-death pathways by activating mitochondrial permeability transition pore formation and causing the release of several proteins, such as cytochrome c and proapoptotic factors. Although the molecular mechanisms for this process are still under investigation, important mitochondrial adaptations have been identified that can inhibit permeability transition activation and prevent apoptosis and necrosis. Specifically, myocardial preconditioning is an intriguing adaptation by which brief ischemia and reperfusion prime the mitochondria so that a subsequent prolonged period of ischemia is better tolerated. Mitochondrial ATP-dependent potassium channels seem to play a critical role in triggering or mediating this protection. The objective of this review is to outline the role of the mitochondria in supporting myocardial energy under normal and ischemic conditions. It will also provide insight into the mechanisms by which mitochondrial signaling in preconditioning can protect the myocyte during subsequent prolonged ischemic periods.
引用
收藏
页码:141 / 148
页数:8
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