Physiological role of mitochondrial Ca2+ transport

Abstract

A model has been proposed in which mitochondrial Ca2+ ion transport serves to regulate mitochondrial matrix free Ca2+ ([Ca2+]m), with the advantage to the animal that this allows the regulation of pyruvate dehydrogenase and the tricarboxylate cycle in response to energy demand. This article examines recent evidence for dehydrogenase activation and for increases in [Ca2+]m in response to increased tissue energy demands, especially in cardiac myocytes and in heart. It critiques recent results on beat-to-beat variation in [Ca2+]m in cardiac muscle and also briefly surveys the impact of mitochondrial Ca2+ transport on transient changes in cytosolic free Ca2+ in excitable tissues. Finally, it proposes that a failure to elevate [Ca2+]m sufficiently in response to work load may underlie some cardiomyopathies of metabolic origin.