Mitochondria and ischemia-reperfusion injury of the heart: Fixing a hole

被引:273
作者
Di Lisa, Fabio
Bernardi, Paolo
机构
[1] Univ Padua, Dipartimento Chim Biol, I-35121 Padua, Italy
[2] Univ Padua, Dipartimento Sci Biomed Sperimentali, I-35121 Padua, Italy
[3] Univ Padua, CNR, Ist Neurosci, I-35121 Padua, Italy
关键词
mitochondria; permeability transition; reactive oxygen species; ischemia; cell death;
D O I
10.1016/j.cardiores.2006.01.016
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Ischemia and post-ischemic reperfusion cause a wide array of functional and structural alterations of mitochondria. Although mitochondrial impairment is recognized as pivotal in determining loss of viability, the causal relationships among the various processes involved is ill defined. Nevertheless, a wide consensus exists in attributing a crucial role to opening of the mitochondrial peemeability transition pore (PTP). Strong support for this concept has recently been provided by the reduced infarct size observed in mice lacking cyclophilin D. This protein located within the mitochondrial matrix favours PTP opening by increasing its sensitivity to Call in a process that is antagonized by cyclosporin A. Genetic approaches have also been used to demonstrate that adenine nucleotide translocase is not an essential component of the PTP. Here, we discuss our current understanding of the structure and function of PTP in the context of heart injury caused by ischemia and reperfusion. (c) 2006 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:191 / 199
页数:9
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