Journal
AUTOPHAGY
Volume 3, Issue 6, Pages 632-634Publisher
LANDES BIOSCIENCE
DOI: 10.4161/auto.4913
Keywords
cardiac hypertrophy; heart failure; cardiomyocyte; beclin 1; cardiac remodeling
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Funding
- NHLBI NIH HHS [R01 HL072016] Funding Source: Medline
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In the setting of hemodynamic stress, such as occurs in hypertension or following OF myocardial infarction, the heart undergoes a compensatory hypertrophic growth response. Left unchecked, this hypertrophic response triggers myocyte death, ventricular dilation, diminished contractile performance, and a clinical syndrome of heart failure. For some years, autophagy has been implicated in heart failure. More recently, mechanistic studies have emerged which provide new insights into the molecular underpinnings of hemodynamic stress-induced cardiomyocyte autophagy. Further, these studies have begun to provide clues as to whether cardiomyocyte autophagy is adaptive, mitigating disease pathogenesis, or maladaptive, contributing to disease progression. Here, we discuss recent studies that both answer some questions and pose new ones.
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