Mitochondrial pathways for ROS formation and myocardial injury: the relevance of p66Shc and monoamine oxidase

被引:136
作者
Di Lisa, Fabio [1 ,2 ,3 ]
Kaludercic, Nina [2 ]
Carpi, Andrea [2 ]
Menabo, Roberta [3 ]
Giorgio, Marco [4 ]
机构
[1] Dip Sci Biomed Sperimentali, I-35121 Padua, Italy
[2] Univ Padua, Dept Biomed Sci, Padua, Italy
[3] CNR, Inst Neurosci, Padua, Italy
[4] European Inst Oncol, Milan, Italy
关键词
Oxidative stress; Mitochondria; p66(Shc); Monoamine oxidase; PERMEABILITY TRANSITION PORE; ISCHEMIA-REPERFUSION INJURY; OXIDATIVE STRESS; NITRIC-OXIDE; SIGNAL-TRANSDUCTION; HEART-FAILURE; CELL-DEATH; LIFE-SPAN; ISCHEMIA/REPERFUSION INJURY; ENDOTHELIAL DYSFUNCTION;
D O I
10.1007/s00395-009-0008-4
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Although mitochondria are considered the most relevant site for the formation of reactive oxygen species (ROS) in cardiac myocytes, a major and unsolved issue is where ROS are generated in mitochondria. Respiratory chain is generally indicated as a main site for ROS formation. However, other mitochondrial components are likely to contribute to ROS generation. Recent reports highlight the relevance of monoamine oxidases (MAO) and p66(Shc). The importance of these systems in the irreversibility of ischemic heart injury will be discussed along with the cardioprotective effects elicited by both MAO inhibition and p66(Shc) knockout. Finally, recent evidence will be reviewed that highlight the relevance of mitochondrial ROS formation also in myocardial failure and atherosclerosis.
引用
收藏
页码:131 / 139
页数:9
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