Demuth K, Myara I, Moatti N
Laboratoire de biochimie, hôpital Broussais, Paris, France.
Ann Biol Clin (Paris). 1995;53(4):171-91.
Through their specific biological properties, vascular endothelial cells play a major role in maintaining the homeostasis of the cardiovascular system. The vascular endothelium participates actively in coagulation and fibrinolysis, contributes to regulating vascular tone, is involved in inflammation and immunological responses, produces several different stromal components, plays a crucial role in angiogenesis and wound-healing, and interacts with plasma lipoproteins. These physiological functions of endothelial cells are triggered by different endothelium derived mediators and are regulated by numerous environmental factors that can markedly modulate the functional state of these cells by affecting their biosynthetic capabilities, giving them different phenotypes in native, activated and injured states. Excessive endothelial activation leads to changes in endothelial cell gene expression, leading to what is referred to as a dysfunctional state. In this non-adaptative functional state, endothelial cells lose the ability to adjust, within the physiological range, some of their constitutive functions and express newly induced molecules, some of which act as proatherosclerotic factors. Activated endothelial cells thus participate actively in the pathogenesis of atherosclerosis.
血管内皮细胞凭借其特定的生物学特性，在维持心血管系统的稳态中发挥着主要作用。血管内皮积极参与凝血和纤维蛋白溶解过程，有助于调节血管张力，参与炎症和免疫反应，产生多种不同的基质成分，在血管生成和伤口愈合中起关键作用，并与血浆脂蛋白相互作用。内皮细胞的这些生理功能由不同的内皮衍生介质触发，并受到众多环境因素的调节，这些环境因素可通过影响其生物合成能力显著调节这些细胞的功能状态，使其在天然、活化和损伤状态下呈现不同的表型。内皮细胞过度活化会导致内皮细胞基因表达发生变化，进而导致所谓的功能失调状态。在这种非适应性功能状态下，内皮细胞失去了在生理范围内调节其某些固有功能的能力，并表达新诱导的分子，其中一些分子充当促动脉粥样硬化因子。因此，活化的内皮细胞积极参与动脉粥样硬化的发病机制。
