The Mitochondrial Permeability Transition Pore and the Cardiac Necrotic Program

被引:29
作者
Baines, Christopher P. [1 ,2 ]
机构
[1] Univ Missouri, Dept Biomed Sci, Dalton Cardiovasc Res Ctr, Columbia, MO 65211 USA
[2] Univ Missouri, Dept Med Pharmacol & Physiol, Dalton Cardiovasc Res Ctr, Columbia, MO 65211 USA
关键词
Apoptosis; Calpain; Cyclophilin-D; Mitochondria; Necrosis; PARP; Permeability transition; Reactive oxygen species; RIP kinases; FOCAL CEREBRAL-ISCHEMIA; CELL-DEATH; REPERFUSION INJURY; CYCLOPHILIN-D; TRANSGENIC MICE; CYCLOSPORINE-A; HEART-FAILURE; MUSCULAR-DYSTROPHY; APOPTOSIS; NECROSIS;
D O I
10.1007/s00246-010-9880-9
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
That apoptosis is mediated by specific pathways has long been established. However, more recent data have begun to suggest that necrosis may in fact be "programmed" and not a default "accidental" pathway as previously thought. The mitochondrial permeability transition pore, a known contributor to the development of many cardiac diseases, is emerging as one among several mediators of this necrotic program. Consequently, this report briefly reviews the roles of necrosis versus apoptosis in the pathogenesis of cardiac disease and discusses the role that the mitochondrial pore plays in cardiac necrotic cell death.
引用
收藏
页码:258 / 262
页数:5
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