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Abstract
As the main source of energy in the body, mitochondria are highly dynamic organelles, which are constantly going through fusion and fission. The fine balance of mitochondrial fusion and fission plays an important role in maintaining the stability of cardiomyocyte homeostasis. The processes of mitochondrial fusion and fission are very complex, which is mediated by fusion and fission proteins. Disruptions in these processes through controlling fusion and fission proteins affect mitochondrial functions and cardiomyocyte survival. Ischemia/reperfusion (I/R) can regulate the expression and post-translational modifications of fusion and fission proteins thereby inducing the abnormality of mitochondrial fusion and fission and cardiomyocyte apoptosis. Furthermore, intervention with the expression and function of fusion and fission proteins influences on cardiomyocyte apoptosis under I/R conditions. In this review, we focus on the current developments in the effects of mitochondrial fusion and fission on cardiomyocyte functions, the implications for cardiomyocyte apoptosis in response to I/R, and possible mechanisms. And we review their roles as a potential therapeutic target for treating I/R-induced cardiomyocyte injury.
Published Version
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