Department of Biomedical Engineering, Indiana University-Purdue University Indianapolis, Indianapolis, IN 46202, USA.
J R Soc Interface. 2011 Oct 7;8(63):1379-85. doi: 10.1098/rsif.2011.0177. Epub 2011 Jul 6.
Blood vessels are under constant mechanical loading from blood pressure and flow which cause internal stresses (endothelial shear stress and circumferential wall stress, respectively). The mechanical forces not only cause morphological changes of endothelium and blood vessel wall, but also trigger biochemical and biological events. There is considerable evidence that physiologic stresses and strains (stretch) exert vasoprotective roles via nitric oxide and provide a homeostatic oxidative balance. A perturbation of tissue stresses and strains can disturb biochemical homeostasis and lead to vascular remodelling and possible dysfunction (e.g. altered vasorelaxation, tone, stiffness, etc.). These distinct biological endpoints are caused by some common biochemical pathways. The focus of this brief review is to point out some possible commonalities in the molecular pathways in response to endothelial shear stress and circumferential wall stretch.
血管不断受到血压和血流产生的机械负荷的影响,从而产生内部应力(分别为内皮剪切力和周向壁应力)。机械力不仅会引起血管内皮和血管壁的形态变化,还会引发生化和生物学事件。有大量证据表明,生理应激和应变(拉伸)通过一氧化氮发挥血管保护作用,并提供体内平衡的氧化平衡。组织应力和应变的改变会扰乱生化内稳态,导致血管重塑和可能的功能障碍(例如,血管舒张、张力、僵硬等改变)。这些不同的生物学终点是由一些共同的生化途径引起的。本文简要回顾的重点是指出对内皮剪切力和周向壁拉伸的分子途径的一些可能的共同点。