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血管紧张素 II,从血管收缩因子到生长因子:一种范式转变。

Angiotensin II, from vasoconstrictor to growth factor: a paradigm shift.

机构信息

From the Division of Cardiology, Department of Medicine, Emory University, Atlanta, GA.

出版信息

Circ Res. 2014 Feb 28;114(5):754-7. doi: 10.1161/CIRCRESAHA.114.303045.

DOI:10.1161/CIRCRESAHA.114.303045
PMID:24577962
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3985550/
Abstract

Angiotensin II (Ang II) is today considered as one of the essential factors in the pathophysiology of cardiovascular disease, producing acute, hemodynamic and chronic, pleiotropic effects. Although now it is widely accepted that these chronic effects are important, Ang II was initially considered only a short-acting, vasoactive hormone. This view was modified a quarter of a century ago when Dr. Owens and his group published a paper in with initial evidence that Ang II can act as a growth factor that regulates cell hypertrophy. They showed in series of elegant experiments that Ang II promotes hypertrophy and hyperploidy of cultured rat aortic smooth muscle cells. However, Ang II had no effect on hyperplasia. These findings led to a paradigm shift in our understanding of the roles of growth factors and vasoactive substances in cardiovascular pathology and helped to redirect basic and clinical renin-angiotensin system research over the next twenty-five years. Ang II is now known to be a pleiotropic hormone that utilizes multiple signaling pathways to influence most processes that contribute to the development and progression of cardiovascular diseases, ranging from hypertrophy, endothelial dysfunction, cardiac remodeling, fibrosis, and inflammation to oxidative stress.

摘要

血管紧张素 II(Ang II)被认为是心血管疾病病理生理学的基本因素之一,可产生急性、血液动力学和慢性、多效性作用。尽管现在广泛认为这些慢性作用很重要,但 Ang II 最初仅被认为是一种短效、血管活性激素。这种观点在四分之一个世纪前被 Dr. Owens 和他的团队发表的一篇论文所改变,该论文初步证明 Ang II 可以作为一种调节细胞肥大的生长因子。他们通过一系列精心设计的实验表明,Ang II 可促进培养的大鼠主动脉平滑肌细胞肥大和超倍性。然而,Ang II 对细胞增生没有影响。这些发现导致了我们对生长因子和血管活性物质在心血管病理学中的作用的理解发生了范式转变,并有助于在接下来的二十五年中重新引导基础和临床肾素-血管紧张素系统研究。现在已知 Ang II 是一种多效性激素,它利用多种信号通路来影响大多数导致心血管疾病发展和进展的过程,从肥大、内皮功能障碍、心脏重构、纤维化和炎症到氧化应激。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0621/3985550/a8e814ab3ada/nihms561225f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0621/3985550/a8e814ab3ada/nihms561225f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0621/3985550/a8e814ab3ada/nihms561225f1.jpg

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