Department of Molecular Biophysics and Physiology, Rush University Medical Center, Chicago, IL 60612, USA.
J Mol Cell Cardiol. 2013 May;58:125-33. doi: 10.1016/j.yjmcc.2012.12.021. Epub 2013 Jan 7.
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.
线粒体钙信号参与细胞能量代谢的调节，线粒体通过其储存 Ca 的能力、塑造胞质 Ca 信号和产生收缩所需的 ATP 参与心脏兴奋-收缩偶联（ECC）。线粒体的内膜配备了精细的 Ca 摄取和外排通道和转运体系统，允许对胞质 Ca 信号进行解码，并将 Ca 储存在线粒体基质隔室中。然而，争议仍然存在，即在跳动的心脏中 ECC 下的快速胞质 Ca 瞬变是否迅速传递到基质隔室，或者是否由线粒体 Ca 转运机制缓慢整合。这篇综述总结了心脏线粒体 Ca 转运和缓冲的既定和新发现，并讨论了支持或反对 ECC 期间线粒体可以快速摄取 Ca 的观点的证据。
