自噬
压力过载
心力衰竭
自噬体
肌肉肥大
心肌肥大
内科学
医学
溶酶体
心脏病学
细胞生物学
生物
生物化学
酶
细胞凋亡
作者
Xuejun Wang,Taixing Cui
出处
期刊:American Journal of Physiology-heart and Circulatory Physiology
[American Physiological Society]
日期:2017-08-01
卷期号:313 (2): H304-H319
被引量:65
标识
DOI:10.1152/ajpheart.00145.2017
摘要
Autophagy is an evolutionarily conserved process used by the cell to degrade cytoplasmic contents for quality control, survival for temporal energy crisis, and catabolism and recycling. Rapidly increasing evidence has revealed an important pathogenic role of altered activity of the autophagosome-lysosome pathway (ALP) in cardiac hypertrophy and heart failure. Although an early study suggested that cardiac autophagy is increased and that this increase is maladaptive to the heart subject to pressure overload, more recent reports have overwhelmingly supported that myocardial ALP insufficiency results from chronic pressure overload and contributes to maladaptive cardiac remodeling and heart failure. This review examines multiple lines of preclinical evidence derived from recent studies regarding the role of autophagic dysfunction in pressure-overloaded hearts, attempts to reconcile the discrepancies, and proposes that resuming or improving ALP flux through coordinated enhancement of both the formation and the removal of autophagosomes would benefit the treatment of cardiac hypertrophy and heart failure resulting from chronic pressure overload.
科研通智能强力驱动
Strongly Powered by AbleSci AI