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血管紧张素 II 与心脏纤维化。

Angiotensin II and Cardiac Fibrosis.

机构信息

Department of Biochemistry and The Cardiovascular Institute, Boston University School of Medicine,Boston, MA 02118,USA.

出版信息

Trends Cardiovasc Med. 1996 Aug;6(6):193-8. doi: 10.1016/S1050-1738(96)00072-2.

Abstract

The renin-angiotensin system has been linked to the pathogenesis of cardiac fibrosis through the use of experimental animal models and by clinical studies. This review emphasizes recent findings implicating the direct action of angiotensin II on cardiac cell types, particularly the cardiac fibroblast, as a causative factor in the development of cardiac fibrosis. The possible influence of other factors acting in concert with angiotensin II either to increase or to attenuate the fibrotic process is also discussed. Nitric oxide is considered as an example of a paracrine agent that can antagonize either the hemodynamic or cellular effects of angiotensin II during both physiological and pathological processes. (Trends Cardiovasc Med 1996;6:193-198).

摘要

肾素-血管紧张素系统通过实验动物模型和临床研究与心肌纤维化的发病机制有关。这篇综述强调了最近的发现,即血管紧张素 II 对心脏细胞类型(特别是心肌成纤维细胞)的直接作用是导致心肌纤维化发展的一个致病因素。还讨论了其他因素与血管紧张素 II 协同作用以增加或减弱纤维化过程的可能影响。一氧化氮被认为是一种旁分泌因子的例子,它可以在生理和病理过程中拮抗血管紧张素 II 的血液动力学或细胞作用。(趋势心血管医学 1996;6:193-198)。

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