Many studies indicate that apoptosis is involved in the progression of congestive heart failure. At present, mechanisms that mitochondria regulates cell apoptosis is widely accepted. Cardiac myocytes have abundant mitochondria, which plays an important role in maintenance of cell physiological function. Recent studies find that cardiac energy metabolic shifts occur as a normal response to diverse physiologic and dietary conditions and as a component of the pathophysiologic processes which accompany cardiac hypertrophy, heart failure, and myocardial ischemia. Both clinical and experimental studies show that cardiac function can be improved and apoptosis is inhibited by intervention in energetic metabolism of myocytes.
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