Physiological and Pathological Roles of the Mitochondrial Permeability Transition Pore in the Heart

被引:352
作者
Kwong, Jennifer Q. [1 ]
Molkentin, Jeffery D. [1 ,2 ]
机构
[1] Univ Cincinnati, Dept Pediat, Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA
[2] Howard Hughes Med Inst, Cincinnati, OH 45229 USA
基金
美国国家卫生研究院;
关键词
PERIPHERAL BENZODIAZEPINE-RECEPTOR; ADENINE-NUCLEOTIDE TRANSLOCASE; CA-2&-INDUCED MEMBRANE TRANSITION; COMPRISE VDAC MOLECULES; DEPENDENT ANION CHANNEL; CYTOCHROME-C RELEASE; CYCLOPHILIN-D; PHOSPHATE-CARRIER; ATP SYNTHASE; CELL-DEATH;
D O I
10.1016/j.cmet.2014.12.001
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Prolonged mitochondrial permeability transition pore (MPTP) opening results in mitochondrial energetic dysfunction, organelle swelling, rupture, and typically a type of necrotic cell death. However, acute opening of the MPTP has a critical physiologic role in regulating mitochondrial Ca2+ handling and metabolism. Despite the physiological and pathological roles that the MPTP orchestrates, the proteins that comprise the pore itself remain an area of ongoing investigation. Here, we will discuss the molecular composition of the MPTP and its role in regulating cardiac physiology and disease. A better understanding of MPTP structure and function will likely suggest novel cardioprotective therapeutic approaches.
引用
收藏
页码:206 / 214
页数:9
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