Mitochondrial research is undergoing something of a renaissance with the discovery that mitochondria are no longer considered to be static, rod-shaped organelles whose only role within the cell is to generate ATP. In fact, mitochondria are highly mobile organelles, capable of changing their shape by undergoing 'fusion' (to form elongated, interconnected mitochondria) and 'fission' (to form fragmented, discrete mitochondria).1'2 Changes in mitochondrial morphology are regulated by the evolutionary conserved mitochondrial fusion proteins, mitofu-sins 1 and 2 (Mfn1 and Mfn2) and optic atrophy-1 (OPA1), and the mitochondrial fission proteins, dynamin-related peptide 1 (Drp1), mitochondrial fission protein 1 (Fis1), mitochondrial fission factor (Mff), and mitochondrial dynamics proteins of 49 and 51 kDa (MiD49/51).1'2 Until recently, the investigation of mitochondrial dynamics and morphology had been largely confined to non-cardiovascular cells. However, a number of recent experimental studies have suggested that changes in mitochondrial morphology may play a role in the cardiovascular system in the settings of vascular smooth cell proliferation, cardiac development and differentiation, stem cell differentiation, myocardial ischaemia-reperfusion injury (IRI), and heart failure (reviewed in 1 and 2).
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