Pathological Ventricular Remodeling: Mechanisms: Part 1 of 2

被引:712
作者
Burchfield, Jana S. [1 ]
Xie, Min [2 ]
Hill, Joseph A. [2 ,3 ]
机构
[1] Texas Heart Inst, Houston, TX 77025 USA
[2] Univ Texas SW Med Ctr Dallas, Dept Internal Med Cardiol, Dallas, TX 75390 USA
[3] Univ Texas SW Med Ctr Dallas, Dept Mol Biol, Dallas, TX 75390 USA
基金
美国国家卫生研究院;
关键词
cardiac electrophysiology; fibrosis; inflammation; stem cells; ventricular remodeling; PRESERVED EJECTION FRACTION; CHRONIC HEART-FAILURE; CARDIOVASCULAR MAGNETIC-RESONANCE; TO-MESENCHYMAL TRANSITION; CARDIAC-HYPERTROPHY; ANGIOTENSIN-II; MYOCARDIAL-INFARCTION; NATRIURETIC PEPTIDE; PROTEIN-KINASE; INTRAVENOUS IMMUNOGLOBULIN;
D O I
10.1161/CIRCULATIONAHA.113.001878
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Despite declines in heart failure morbidity and mortality with current therapies, rehospitalization rates remain distressingly high, substantially affecting individuals, society, and the economy. As a result, the need for new therapeutic advances and novel medical devices is urgent. Disease-related left ventricular remodeling is a complex process involving cardiac myocyte growth and death, vascular rarefaction, fibrosis, inflammation, and electrophysiological remodeling. Because these events are highly interrelated, targeting a single molecule or process may not be sufficient. Here, we review molecular and cellular mechanisms governing pathological ventricular remodeling.
引用
收藏
页码:388 / 400
页数:13
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