Apoptosis in heart failure represents programmed cell survival, not death, of cardiomyocytes and likelihood of reverse remodeling.
Apoptosis is a highly orchestrated form of programmed cell death, and this is believed to contribute to continuous decline of ventricular function in heart failure. However, the apoptotic cascade is not completed in failing myocardium and DNA damage is prevented due to abolition of DNA fragmentation factors. The extranuclear apoptotic program is interrupted secondary to inhibition of activated caspase-3 by upregulated inhibitors of apoptotic process. During the apoptotic process, upstream step comprising extensive mitochondrial loss of cytochrome c may contribute to systolic dysfunction of heart. Intactness of nuclear blueprint underscores the likelihood of reverse remodeling that has been demonstrated in the post-LVAD myocardial specimens.
Haider
Nezam
N
Drexel University College of Medicine, Philadelphia, Pennsylvania, USA.
Narula
Navneet
N
Narula
Jagat
J
D000818:Animals; D017209:Apoptosis; D053148:Caspase 3; D053181:Caspase 8; D053453:Caspase 9; D020169:Caspases / Q000502:physiology; D004792:Enzyme Precursors / Q000502:physiology; D005260:Female; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D008297:Male; D032383:Myocytes, Cardiac / Q000502:physiology*; D020257:Ventricular Remodeling
D004792:Enzyme Precursors; C505407:CASP3 protein, human; C505530:CASP8 protein, human; C506433:CASP9 protein, human; D053148:Caspase 3; D053181:Caspase 8; D053453:Caspase 9; D020169:Caspases