舒张功能障碍的分子基础。
Molecular basis of diastolic dysfunction.
作者信息
Periasamy Muthu, Janssen Paul M L
机构信息
Davis Heart and Lung Research Institute, The Ohio State University, Columbus OH, USA.
出版信息
Heart Fail Clin. 2008 Jan;4(1):13-21. doi: 10.1016/j.hfc.2007.10.007.
Abstract
Diastolic dysfunction is characterized by prolonged relaxation, increased filling pressure, decreased contraction velocity, and reduced cardiac output. Phenotypical features of diastolic dysfunction can be observed at the level of the isolated myocyte. This article reviews the cellular mechanisms that control relaxation at the level of the myocyte in the healthy situation and discusses the alterations that can affect physiologic function during disease. It focuses specifically on the mechanisms that regulate intracellular calcium handling, and the response of the myofilaments to calcium, including the changes in these components that can contribute to diastolic dysfunction.
摘要
舒张功能障碍的特征是舒张期延长、充盈压升高、收缩速度降低和心输出量减少。在单个心肌细胞水平上可以观察到舒张功能障碍的表型特征。本文回顾了健康状态下心肌细胞水平控制舒张的细胞机制，并讨论了疾病期间可能影响生理功能的改变。它特别关注调节细胞内钙处理的机制，以及肌丝对钙的反应，包括这些成分中可能导致舒张功能障碍的变化。
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