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Regulation of mitochondrial Ca2+ and its effects on energetics and redox balance in normal and failing heart Liu T; O'Rourke BJ Bioenerg Biomembr 2009[Apr]; 41 (2): 127-32Ca(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+)](m)) uptake remains unclear, and we review the debate on this subject in this article. [Ca(2+)](m) 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+)](m) 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+)](m) accumulation.|*Citric Acid Cycle[MESH]|*Oxidative Phosphorylation[MESH]|Adenosine Triphosphate/*biosynthesis[MESH]|Animals[MESH]|Calcium[MESH]|Heart Failure/*metabolism[MESH]|Humans[MESH]|Mitochondria, Heart/*metabolism/pathology[MESH]|Mitochondrial ADP, ATP Translocases/metabolism[MESH]|Myocardium/*metabolism/pathology[MESH]|NAD/biosynthesis[MESH]|Oxidation-Reduction[MESH]|Proton-Translocating ATPases/metabolism[MESH]|Reactive Oxygen Species/metabolism[MESH]|Sodium/metabolism[MESH] |
