作者: Stephan Huveneers , Mat J.A.P. Daemen , Peter L. Hordijk
DOI: 10.1161/CIRCRESAHA.116.305720
关键词:
摘要: Vascular stiffness is a mechanical property of the vessel wall that affects blood pressure, permeability, and inflammation. As result, vascular key driver (chronic) human disorders, including pulmonary arterial hypertension, kidney disease, atherosclerosis. Responses endothelium to stiffening involve integration cues from various sources, extracellular matrix, smooth muscle cells, forces derive shear stress blood. This response in turn endothelial cell contractility, which an important regulates stiffness, leukocyte-vessel interactions. Moreover, reduces nitric oxide production, promotes contraction vasoconstriction. In fact, stiffening, microcirculatory dysfunction, precedes hypertension thus underlies development disease. Here, we review cross talk among controlled by Rho-driven actomyosin contractility cellular mechanotransduction. addition discussing inputs relevant molecular events endothelium, address actomyosin-regulated changes at adhesion complexes are genetically associated with cardiovascular Finally, discuss recent findings broaden therapeutic options for targeting this signaling pathway pathogenesis.