作者: Beverly A. Rothermel , Joseph A. Hill
DOI: 10.4161/AUTO.4913
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摘要: In the setting of hemodynamic stress, such as occurs in hypertension or following myocardial infarction, heart undergoes a compensatory hypertrophic growth response. Left unchecked, this response triggers myocyte death, ventricular dilation, diminished contractile performance, and clinical syndrome failure. For some years, autophagy has been implicated More recently, mechanistic studies have emerged which provide new insights into molecular underpinnings stress-induced cardiomyocyte autophagy. Further, these begun to clues whether is adaptive, mitigating disease pathogenesis, maladaptive, contributing progression. Here, we discuss recent that both answer questions pose ones.