The Ins and Outs of Mitochondrial Calcium

被引：222

作者：

Finkel, Toren ^{[1
]}

Menazza, Sara ^{[2
]}

Holmstroem, Kira M. ^{[1
]}

Parks, Randi J. ^{[2
]}

Liu, Julia ^{[1
]}

Sun, Junhui ^{[2
]}

Liu, Jie ^{[1
]}

Pan, Xin ^{[3
]}

Murphy, Elizabeth ^{[2
]}

机构：

[1] NHLBI, Ctr Mol Med, NIH, Bethesda, MD 20892 USA

[2] NHLBI, Syst Biol Ctr, NIH, Bethesda, MD 20892 USA

[3] Natl Ctr Biomed Anal, Cell Biol Lab, Beijing, Peoples R China

来源：

CIRCULATION RESEARCH | 2015年 / 116卷 / 11期

关键词：

calcium signaling; cell death; mitochondria; PERMEABILITY TRANSITION PORE; HEART-MITOCHONDRIA; CA2+ UPTAKE; OXIDATIVE-PHOSPHORYLATION; ESSENTIAL COMPONENT; CYCLOSPORINE-A; ISCHEMIA/REPERFUSION INJURY; CARDIAC MITOCHONDRIA; REPERFUSION INJURY; UNIPORTER;

D O I：

10.1161/CIRCRESAHA.116.305484

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Calcium is thought to play an important role in regulating mitochondrial function. Evidence suggests that an increase in mitochondrial calcium can augment ATP production by altering the activity of calcium-sensitive mitochondrial matrix enzymes. In contrast, the entry of large amounts of mitochondrial calcium in the setting of ischemia-reperfusion injury is thought to be a critical event in triggering cellular necrosis. For many decades, the details of how calcium entered the mitochondria remained a biological mystery. In the past few years, significant progress has been made in identifying the molecular components of the mitochondrial calcium uniporter complex. Here, we review how calcium enters and leaves the mitochondria, the growing insight into the topology, stoichiometry and function of the uniporter complex, and the early lessons learned from some initial mouse models that genetically perturb mitochondrial calcium homeostasis.

引用

页码：1810 / 1819

页数：10

共 79 条

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