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

Abstract

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-β in both thoracic and abdominal aortic aneurysms have been the focus of recent studies. While these studies have demonstrated profound effects of manipulating TGF-β 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-β in the development of aortic aneurysms.

Figure 1. Schematic summary of the main concepts discussed in this brief review

AngII and TGF-β have potential interactions in both Smad- and ERK-related signaling pathways [2,3]. While AngII plays a critical role in the formation of aortic aneurysms [,–,–35], there are also potential contributions of TGF-β to aortic aneurysmal development [3,16,18,19,26,34].