Regulation Of Cardiomyocyte Apoptosis

The stimulus for cardiomyocyte apoptosis clearly depends upon the clinical or experimental setting. Ischaemia is associated with many changes in the intracellular and extracellular milieu of cardiomyocytes, many of which are potent apoptotic stimuli. Thus, hypoxia promotes cardiomyocyte apoptosis, both in vitro and in vivo, and ischaemia/reperfusion and hypoxia/reoxygenation are associated with increased expression of Fas. Decreased serum and glucose concentrations trigger cytochrome c release from mitochondria in cardiomyo-cytes, suggesting that ischaemia induced apoptosis may be mediated by mitochondrial amplification. Indeed oxygen species promote apoptosis by triggering pathways involving mitochondrial release of cytochrome c and caspase activation.

Catecholamines/ATII Mechanical stress

Ischaemia/reperfusio

Caspase 8 cleavage

Catecholamines/ATII Mechanical stress

Ischaemia/reperfusio

Cardiomyocyte Apoptosis

Survival factor Withdrawal

Caspase cascade

Procaspase 9

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