Pathophysiological effects of RhoA and Rho-associated kinase on cardiovascular system

被引：43

作者：

Cai, Anping ^{[1
]}

Li, Liwen ^{[1
]}

Zhou, Yingling ^{[1
]}

机构：

[1] Guangdong Acad Med Sci, Guangdong Gen Hosp, Guangdong Prov Key Lab Coronary Heart Dis Prevent, Dept Cardiol,Guangdong Cardiovasc Inst, 106 Zhongshan Rd 2, Guangzhou 510080, Guangdong, Peoples R China

来源：

JOURNAL OF HYPERTENSION | 2016年 / 34卷 / 01期

关键词：

cardiovascular system; ras homolog gene family; member A; ras homolog gene family-associated kinase; VASCULAR SMOOTH-MUSCLE; NITRIC-OXIDE SYNTHASE; LONG-TERM INHIBITION; INDUCED HYPERTROPHIC RESPONSES; IMPROVES ENDOTHELIAL FUNCTION; INDUCED DOWN-REGULATION; ACUTE ISCHEMIC-STROKE; SMALL G-PROTEINS; ANGIOTENSIN-II; CARDIAC MYOCYTES;

D O I：

10.1097/HJH.0000000000000768

中图分类号：

R6 [外科学];

学科分类号：

1002 ; 100210 ;

摘要：

In past decades, growing evidence from basic and clinical researches reveal that small guanosine triphosphate binding protein ras homolog gene family, member A (RhoA) and its main effector Rho-associated kinase (ROCK) play central and complex roles in cardiovascular systems, and increasing RhoA and ROCK activity is associated with a broad range of cardiovascular diseases such as congestive heart failure, atherosclerosis, and hypertension. Favorable outcomes have been observed with ROCK inhibitors treatment. In this review, we briefly summarize the pathophysiological roles of RhoA/ROCK signaling pathway on cardiovascular system, displaying the potential benefits in the cardiovascular system with controlling RhoA/ROCK signaling pathway.

引用

页码：3 / 10

页数：8

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