Lehoux S, Tedgui A
INSERM U141, Paris, France.
Hypertension. 1998 Aug;32(2):338-45. doi: 10.1161/01.hyp.32.2.338.
The vascular wall is constantly subjected to a variety of mechanical forces in the form of stretch (tensile stress), due to blood pressure, and shear stress, due to blood flow. Alterations in either of these stresses are known to result in vascular remodeling, an adaptation characterized by modified morphology and function of the blood vessels, allowing the vessels to cope with physiological or pathological conditions. The processes involved in vascular remodeling include cellular hypertrophy and hyperplasia, as well as enhanced protein synthesis or extracellular matrix protein reorganization. In vitro studies using vascular cells have attempted to identify the mechanisms behind structural alterations. Possible pathways include ion channels, integrin interaction between cells and the extracellular matrix, activation of various tyrosine kinases (such as c-Src, focal adhesion kinase, and mitogen-activated protein kinases), and autocrine production and release of growth factors. These pathways lie upstream of de novo synthesis of immediate response genes and total protein synthesis, both of which are likely to be involved in the process of vascular remodeling.
血管壁持续受到各种机械力的作用，以拉伸（拉应力）的形式，这是由血压引起的；还有剪切应力，这是由血流引起的。已知这些应力中的任何一种改变都会导致血管重塑，这是一种以血管形态和功能改变为特征的适应性变化，使血管能够应对生理或病理状况。血管重塑所涉及的过程包括细胞肥大和增生，以及蛋白质合成增强或细胞外基质蛋白重组。使用血管细胞的体外研究试图确定结构改变背后的机制。可能的途径包括离子通道、细胞与细胞外基质之间的整合素相互作用、各种酪氨酸激酶（如c-Src、粘着斑激酶和丝裂原活化蛋白激酶）的激活，以及生长因子的自分泌产生和释放。这些途径位于即时反应基因的从头合成和总蛋白质合成的上游，而这两者都可能参与血管重塑过程。
