Abstract
Calcium ion (Ca(2+)) plays a critical role in the cardiac mitochondria function. Ca(2+) entering the mitochondria is necessary for ATP production and the contractile activity of cardiomyocytes. However, excessive Ca(2+) in the mitochondria results in mitochondrial dysfunction and cell death. Mitochondria maintain Ca(2+) homeostasis in normal cardiomyocytes through a comprehensive regulatory mechanism by controlling the uptake and release of Ca(2+) in response to the cellular demand. Understanding the mechanism of modulating mitochondrial Ca(2+) homeostasis in the cardiomyocyte could bring new insights into the pathogenesis of cardiac disease and help developing the strategy to prevent the heart from damage at an early stage. In this review, we summarized the latest findings in the studies on the cardiac mitochondrial Ca(2+) homeostasis, focusing on the regulation of mitochondrial calcium uptake, which acts as a double-edged sword in the cardiac function. Specifically, we discussed the dual roles of mitochondrial Ca(2+) in mitochondrial activity and the impact on cardiac function, the molecular basis and regulatory mechanisms, and the potential future research interest.