Calcium signaling in cardiac mitochondria

被引:72
|
作者
Dedkova, Elena N. [1 ]
Blatter, Lothar A. [1 ]
机构
[1] Rush Univ, Med Ctr, Dept Mol Biophys & Physiol, Chicago, IL 60612 USA
基金
美国国家卫生研究院;
关键词
Excitation-contraction coupling; Heart; Intracellular calcium; Mitochondrial Ca transport; Ca buffering; PERMEABILITY TRANSITION PORE; RAT VENTRICULAR MYOCYTES; TO-BEAT OSCILLATIONS; CA2+ UPTAKE; HEART-MITOCHONDRIA; SARCOPLASMIC-RETICULUM; OXIDATIVE-PHOSPHORYLATION; RYANODINE RECEPTOR; ESSENTIAL COMPONENT; INORGANIC POLYPHOSPHATE;
D O I
10.1016/j.yjmcc.2012.12.021
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Mitochondrial Ca signaling contributes to the regulation of cellular energy metabolism, and mitochondria participate in cardiac excitation-contraction coupling (ECC) through their ability to store Ca, shape the cytosolic Ca signals and generate ATP required for contraction. The mitochondrial inner membrane is equipped with an elaborate system of channels and transporters for Ca uptake and extrusion that allows for the decoding of cytosolic Ca signals, and the storage of Ca in the mitochondrial matrix compartment. Controversy, however remains whether the fast cytosolic Ca transients underlying ECC in the beating heart are transmitted rapidly into the matrix compartment or slowly integrated by the mitochondrial Ca transport machinery. This review summarizes established and novel findings on cardiac mitochondrial Ca transport and buffering, and discusses the evidence either supporting or arguing against the idea that Ca can be taken up rapidly by mitochondria during ECC. This article is part of a Special Issue entitled "Calcium Signaling in Heart". (C) 2013 Elsevier Ltd. All rights reserved.
引用
收藏
页码:125 / 133
页数:9
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