Molecular basis of diastolic dysfunction.
Molecular basis of diastolic dysfunction.
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DOI：
10.1016/j.hfc.2007.10.007
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发表时间：
2008-01-01
影响因子：
3.4
通讯作者：
Janssen, Paul M L
中科院分区：
文献类型：
--
作者：
Periasamy, Muthu;Janssen, Paul M L
舒张功能障碍的特征是舒张时间延长、充盈压升高、收缩速度降低和心输出量减少。舒张功能障碍的表型特征可以在分离的心肌细胞水平上观察到。本文综述了在健康情况下，在肌细胞水平上控制松弛的细胞机制，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，包括可能导致舒张功能障碍的这些成分的变化。
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.