Endothelial mechanosensing: A forgotten target to treat vascular remodeling in hypertension?

被引:5
|
作者
Tiezzi, Margherita [1 ,2 ]
Deng, Hanqiang [3 ]
Baeyens, Nicolas [4 ]
机构
[1] Univ Libre Bruxelles, Erasmus Hosp, Cardiol Dept, Brussels, Belgium
[2] Univ Libre Bruxelles, Inflammat & Cell Death Signalling Lab, Brussels, Belgium
[3] Yale Univ, Yale Cardiovasc Res Ctr, Dept Internal Med, Sch Med, New Haven, CT USA
[4] Univ Libre Bruxelles, Lab Physiol & Pharmacol, Brussels, Belgium
关键词
Mechanotransduction; Blood flow; Shear stress; Vascular remodeling; Pulmonary hypertension; Systemic hypertension; EndMT; TGF-beta signaling; BMP9; FLUID SHEAR-STRESS; PULMONARY ARTERIAL-HYPERTENSION; TO-MESENCHYMAL TRANSITION; CAPILLARY RAREFACTION; BLOOD-PRESSURE; GROWTH-FACTOR; NITRIC-OXIDE; VE-CADHERIN; CELLS; FLOW;
D O I
10.1016/j.bcp.2022.115290
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The endothelium is a mechanosensitive organ whose pleiotropic actions regulate vessel structure to adjust tissue perfusion. To do so, it possesses ion channels, receptor complexes, and signaling pathways responding to blood flow, whose activation will either maintain vascular integrity and quiescence or, on the contrary, remodel the vessel's structure in both health and disease. Recent studies have demonstrated the crucial role of endothelial inflammation, endothelial to mesenchymal transition (EndMT), and perturbed hemodynamics in the progression of pulmonary arterial hypertension and essential hypertension. These two distinct diseases share some common mechanistic cues, pointing towards new potential therapeutic approaches to treat them. In this review, we summarize these common mechanisms to map future drug development strategies targeting flow sensing mechanisms and vascular remodeling.
引用
收藏
页数:16
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