Conundrum of angiotensin II and TGF-β interactions in aortic aneurysms

被引：49

作者：

Chen, Xiaofeng ^{[1
]}

Lu, Hong ^{[1
]}

Rateri, Debra L. ^{[1
]}

Cassis, Lisa A. ^{[2
]}

Daugherty, Alan ^{[1
]}

机构：

[1] Univ Kentucky, Saha Cardiovasc Res Ctr, Lexington, KY 40536 USA

[2] Univ Kentucky, Dept Mol & Biomed Pharmacol, Lexington, KY 40536 USA

来源：

CURRENT OPINION IN PHARMACOLOGY | 2013年 / 13卷 / 02期

基金：

美国国家卫生研究院;

关键词：

SMOOTH-MUSCLE-CELLS; MARFAN-SYNDROME; MOUSE MODEL; RECEPTOR; MICE; LOSARTAN; SYSTEM; GAMMA; PROGRESSION; INHIBITION;

D O I：

10.1016/j.coph.2013.01.002

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Angiotensin II (AngII) has been invoked as a principal mediator for the development and progression of both thoracic and abdominal aortic aneurysms. While there is consistency in experimental and clinical studies that overactivation of the renin angiotensin system promotes aortic aneurysm development, there are many unknowns regarding the mechanistic basis underlying AngII-induced aneurysms. Interactions of AngII with TGF-beta in both thoracic and abdominal aortic aneurysms have been the focus of recent studies. While these studies have demonstrated profound effects of manipulating TGF-beta activity on AngII-induced aortic aneurysms, they have also led to more questions regarding the interactions between AngII and this multifunctional cytokine. This review compiled the recent literature to provide insights into understanding the potentially complex interactions between AngII and TGF-beta in the development of aortic aneurysms.

引用

页码：180 / 185

页数：6

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