Metabolic Regulation of Mitochondrial Dynamics and Cardiac Function

Increasing lines of evidence highlight cardiac mitochondria as key regu lators of myocardial function and arrhythmias in response to acute injury and chronic diseases. In recent years, mitochondria have been shown to form highly dynamic organelles that continuously fuse and divide. These morphological changes, caused by complex fusion and fission events, are essential for normal embryonic development as well as other fundamental processes. Disruption of the balance between mitochondrial fusion and fission results in either highly interconnected mitochondrial networks (favoring fusion) or abnormally fragmented mitochondria (favoring fission). Our understanding of these opposing processes has been mark edly advanced by the identification of key proteins that regulate mitochondrial dynamics. Until recently, however, the functional importance of these proteins to the pathogenesis of cardiovascular disorders has received little attention. In this chapter, we discuss recent advances in our understanding of how altered regulation and expression of pro-fusion and pro-fission mitochondrial dynamics proteins impact cardiac function in common cardiovascular diseases.