心力衰竭时细胞内钙离子处理的改变。
Altered intracellular Ca2+ handling in heart failure.
作者信息
Yano Masafumi, Ikeda Yasuhiro, Matsuzaki Masunori
机构信息
Department of Medical Bioregulation, Division of Cardiovascular Medicine, Yamaguchi University School of Medicine, Yamaguchi, Japan.
出版信息
J Clin Invest. 2005 Mar;115(3):556-64. doi: 10.1172/JCI24159.
Abstract
Structural and functional alterations in the Ca2+ regulatory proteins present in the sarcoplasmic reticulum have recently been shown to be strongly involved in the pathogenesis of heart failure. Chronic activation of the sympathetic nervous system or of the renin-angiotensin system induces abnormalities in both the function and structure of these proteins. We review here the considerable body of evidence that has accumulated to support the notion that such abnormalities contribute to a defectiveness of contractile performance and hence to the progression of heart failure.
摘要
最近研究表明，肌浆网中存在的钙离子调节蛋白的结构和功能改变与心力衰竭的发病机制密切相关。交感神经系统或肾素 - 血管紧张素系统的慢性激活会导致这些蛋白的功能和结构出现异常。我们在此回顾大量已积累的证据，这些证据支持这样一种观点，即此类异常会导致收缩功能缺陷，进而促使心力衰竭的进展。
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