Mitochondrial Ca2+ and the heart

It is now well established that mitochondria accumulate Ca2+ ions during cytosotic Ca2+ ([Ca2+](i)) elevations in a variety of cell types including cardiomyocytes. Elevations in intramitochondrial Ca2+ ([Ca2+](m)) activate several key enzymes in the mitochondrial matrix to enhance ATP production, alter the spatial and temporal profile of intracellular Ca2+ signaling, and play an important role in the initiation of cell death pathways. Moreover, mitochondrial Ca2+ uptake stimulates nitric oxide (NO) production by mitochondria, which modulates oxygen consumption, ATP production, reactive oxygen species (ROS) generation, and in turn provides negative feedback for the regulation of mitochondrial Ca2+ accumulation. Controversy remains, however, whether in cardiac myocytes mitochondrial Ca2+ transport mechanisms allow beat-to-beat transmission of fast cytosotic [Ca2+], oscillations into oscillatory changes in mitochondrial matrix [Ca2+](m). This review critically summarizes the recent experimental work in this field. (c) 2007 Elsevier Ltd. All rights reserved.