期刊
JOURNAL OF BIOENERGETICS AND BIOMEMBRANES
卷 41, 期 2, 页码 127-132出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10863-009-9216-8
关键词
Mitochondrial Ca2+ handling; Cardiac energy metabolism; Redox balance; Oxidative phosphorylation; Heart failure
资金
- NIH [P01 HL081427]
Ca2+ has been well accepted as a signal that coordinates changes in cytosolic workload with mitochondrial energy metabolism in cardiomyocytes. During increased work, Ca2+ is accumulated in mitochondria and stimulates ATP production to match energy supply and demand. The kinetics of mitochondrial Ca2+ ([Ca2+](m)) uptake remains unclear, and we review the debate on this subject in this article. [Ca2+](m) has multiple targets in oxidative phosphorylation including the F1/FO ATPase, the adenine nucleotide translocase, and Ca2+-sensitive dehydrogenases (CaDH) of the tricarboxylic acid (TCA) cycle. The well established effect of [Ca2+](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 [Ca2+](m) accumulation.
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