Cardiomyocyte Apoptosis in Experimental Health Failure

摘要: Heart failure is characterized by progressive worsening of left ventricular (LV) function over time. The mechanism(s) responsible for this hemodynamic deterioration are not known. It often assumed, but no means established, that LV dysfunction results largely from ongoing loss functional cardiac units. If myocyte occurs during the course evolving heart and can indeed account dysfunction, then identification factors muscle mass potentially lead to novel therapeutic modalities aimed at preventing transition toward intractable failure. Recent studies in experimental animals have shown through apoptosis, or programmed cell death, 1) following myocardial infarction, 2) presence hypertrophy, 3) aging heart, 4) setting chronic observation apoptosis animal models has since been confirmed failed human heart. Considerable work also accomplished, credible concepts advanced, an attempt uncover physiological molecular triggers While, present, one comfortably accept existence phenomenon failing two integral questions remain essentially unanswered. First, what pathophysiological factors(s), inherent failure, trigger apoptosis? Second, how important progression overt failure? present article will summarize our current knowledge based on data available