Liu Ting, O'Rourke Brian
Institute of Molecular Cardiobiology, Division of Cardiology, The Johns Hopkins University, Baltimore, MD, USA.
J Bioenerg Biomembr. 2009 Apr;41(2):127-32. doi: 10.1007/s10863-009-9216-8.
Ca(2+) has been well accepted as a signal that coordinates changes in cytosolic workload with mitochondrial energy metabolism in cardiomyocytes. During increased work, Ca(2+) is accumulated in mitochondria and stimulates ATP production to match energy supply and demand. The kinetics of mitochondrial Ca(2+) (Ca(2+)) uptake remains unclear, and we review the debate on this subject in this article. Ca(2+) has multiple targets in oxidative phosphorylation including the F1/FO ATPase, the adenine nucleotide translocase, and Ca(2+)-sensitive dehydrogenases (CaDH) of the tricarboxylic acid (TCA) cycle. The well established effect of Ca(2+) is to activate CaDHs of the TCA cycle to increase NADH production. Maintaining NADH level is not only critical to keep a high oxidative phosphorylation rate during increased cardiac work, but is also necessary for the reducing system of the cell to maintain its reactive oxygen species (ROS) -scavenging capacity. Further, we review recent data demonstrating the deleterious effects of elevated Na(+) in cardiac pathology by blunting Ca(2+) accumulation.
钙离子（Ca(2+)）作为一种信号，能够协调心肌细胞胞质工作负荷的变化与线粒体能量代谢，这一点已得到广泛认可。在工作负荷增加期间，Ca(2+)会在线粒体中积累，并刺激ATP生成，以匹配能量供需。线粒体Ca(2+)（Ca(2+)）摄取的动力学仍不清楚，我们将在本文中回顾关于这一主题的争论。Ca(2+)在氧化磷酸化中有多个作用靶点，包括F1/FO ATP酶、腺嘌呤核苷酸转位酶以及三羧酸（TCA）循环中的Ca(2+)敏感脱氢酶（CaDH）。Ca(2+)的一个已被充分证实的作用是激活TCA循环的CaDH，以增加NADH的生成。维持NADH水平不仅对于在心脏工作负荷增加时保持高氧化磷酸化速率至关重要，而且对于细胞的还原系统维持其活性氧（ROS）清除能力也是必要的。此外，我们还回顾了近期的数据，这些数据表明在心脏病理状态下，升高的钠离子（Na(+)）通过抑制Ca(2+)积累而产生有害影响。
