Interplay between the cardiac renin angiotensin system and JAK-STAT signaling: Role in cardiac hypertrophy, ischemia/reperfusion dysfunction, and heart failure
Interplay between the cardiac renin angiotensin system and JAK-STAT signaling: Role in cardiac hypertrophy, ischemia/reperfusion dysfunction, and heart failure
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DOI：
10.1006/jmcc.2002.2076
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发表时间：
2002-11-01
影响因子：
5
通讯作者：
Baker, KM
中科院分区：
文献类型：
--
作者：
Booz, GW;Day, JNE;Baker, KM
G. W. Booz. J. N. E.戴和K。M.贝克心脏肾素血管紧张素系统和JAK-STAT信号之间的相互作用：在心脏肥大、缺血/再灌注功能障碍和心力衰竭中的作用。分子和细胞心脏病学杂志（2002）34，1443-1453。最近的研究表明JAK-STAT信号通路在心脏病理生理学中起着核心作用。JAK-STAT信号转导与压力超负荷诱导的心脏肥大和重塑、缺血预处理和缺血/再灌注诱导的心功能障碍有关。在心肌细胞中表达的不同STAT家族成员似乎与不同的，有时是相反的反应有关，例如细胞生长/存活和凋亡。因此，G蛋白偶联受体激动剂如血管紧张素II对STAT蛋白的差异激活和/或选择性抑制可能导致缺血和心力衰竭期间的心功能障碍。此外，JAK-STAT信号传导可能代表血管紧张素II产生的自分泌环的一个分支，其用于放大血管紧张素II对心肌的作用。本文的目的是提供一个概述，最近的研究结果，已经在心肌细胞JAK-STAT信号，并强调一些未解决的问题，为未来的调查。本综述的中心焦点是最近的研究表明，ANG II对JAK-STAT信号的调节或激活对心脏功能具有病理后果。(C)2002年由Elsevier Science Ltd.出版
G. W. Booz. J. N. E. DAY AND K. M. BAKER. Interplay Between the Cardiac Renin Angiotensin System and JAK-STAT Signaling: Role in Cardiac Hypertrophy, Ischemia/Reperfusion Dysfunction, and Heart Failure. Journal of Molecular and Cellular Cardiology (2002) 34, 1443-1453. Recent studies have shown that the JAK-STAT signaling pathway plays a central role in cardiac pathophysiology. JAK-STAT signaling has been implicated in pressure overload-induced cardiac hypertrophy and remodeling, ischemic preconditioning, and ischemia/reperfusion-induced cardiac dysfunction. The different STAT family members expressed in cardiac myocytes appear to be linked to different, and at times, opposite responses, such as cell growth/survival and apoptosis. Thus, differential activation and/or selective inhibition of the STAT proteins by agonists for G-protein coupled receptors, such as angiotensin II, may contribute to cardiac dysfunction during ischemia and heart failure. In addition, JAK-STAT signaling may represent one limb of an, autocrine loop for angiotensin II generation, that serves to amplify the actions of angiotensin II on cardiac muscle. The purpose of this article is to provide an overview of recent findings that have been made for JAK-STAT signaling in cardiac myocytes and to highlight some unresolved issues for future investigation. The central focus of this review is on recent studies suggesting that modulation or activation of JAK-STAT signaling by ANG II has pathological consequences for heart function. (C) 2002 Published by Elsevier Science Ltd.