期刊
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
卷 51, 期 4, 页码 584-593出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2011.06.010
关键词
Heart failure; Cardiac hypertrophy; Remodeling; Autophagy; Plasticity; HDAC inhibitors; Hypertrophy; AMPK; IP3; mTOR; PKA; p53
资金
- NIH [HL-075173, HL-080144, HL-090842]
- AHA [0640084N]
- ADA [7-08-MN-21-ADA]
- AHA-Jon Holden DeHaan Foundation [0970518N]
- Fondo Nacional de Desarrollo Cientifico y Tecnologico, Chile [FONDECYT 1080436, FONDAP 15010006]
The epidemic of heart failure continues apace, and development of novel therapies with clinical efficacy has lagged. Now, important insights into the molecular circuitry of cardiovascular autophagy have raised the prospect that this cellular pathway of protein quality control may be a target of clinical relevance. Whereas basal levels of autophagy are required for cell survival, excessive levels - or perhaps distinct forms of autophagic flux - contribute to disease pathogenesis. Our challenge will be to distinguish mechanisms that drive adaptive versus maladaptive autophagy and to manipulate those pathways for therapeutic gain. Recent evidence suggests this may be possible. Here, we review the fundamental biology of autophagy and its role in a variety of forms of cardiovascular disease. We discuss ways in which this evolutionarily conserved catabolic mechanism can be manipulated, discuss studies presently underway in heart disease, and provide our perspective on where this exciting field may lead in the future. This article is part of a special issue entitled Key Signaling Molecules in Hypertrophy and Heart Failure. (C) 2011 Elsevier Ltd. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据