Badimon L, Martínez-González J, Llorente-Cortés V, Rodríguez C, Padró T
Cardiovascular Research Center, CSIC- ICCC, Hospital de la Santa CreuISant Pau, Barcelona, Spain.
Curr Mol Med. 2006 Aug;6(5):439-56. doi: 10.2174/156652406778018725.
Atherosclerosis is an inflammatory process, triggered by the presence of lipids in the vascular wall, and encompasses a complex interaction among inflammatory cells, vascular elements, and lipoproteins through expression of several adhesion molecules and cytokines. Subendothelial retention of lipoproteins is the key initiating event in atherosclerosis, provoking a cascade of events to pathogenic response. High levels of plasma lipids, particularly low-density (LDL) and very-low-density lipoproteins (VLDL) are among the pathophysiologic stimuli that induce endothelial dysfunction. Endothelial cells regulate coagulation, thrombosis and the fibrinolytic system; the endothelium modulates the activity of smooth muscle cells (vascular tone/proliferation) and controls the traffic of macromolecules and inflammatory cells to the vessel wall. Furthermore, LDLs have been implicated in the induction of changes in permeability, cell adhesion and secretion of vasoactive molecules (nitric oxide [NO]), while VLDLs seem to modulate the fibrinolytic system [tissue plasminogen activator (TPA) and plasminogen activator inhibitor-1 (PAI-1)]. In this review, we will focus on the pathophysiologic functions of lipoproteins in the vascular wall.
动脉粥样硬化是一种炎症过程，由血管壁中脂质的存在引发，涉及炎症细胞、血管成分和脂蛋白之间通过多种黏附分子和细胞因子的表达而产生的复杂相互作用。脂蛋白在内皮下的潴留是动脉粥样硬化的关键起始事件，引发一系列导致致病反应的事件。血浆脂质水平升高，尤其是低密度脂蛋白（LDL）和极低密度脂蛋白（VLDL），是诱导内皮功能障碍的病理生理刺激因素之一。内皮细胞调节凝血、血栓形成和纤维蛋白溶解系统；内皮调节平滑肌细胞的活性（血管张力/增殖），并控制大分子和炎症细胞向血管壁的转运。此外，LDLs与通透性改变、细胞黏附以及血管活性分子（一氧化氮[NO]）的分泌有关，而VLDLs似乎调节纤维蛋白溶解系统[组织纤溶酶原激活物（TPA）和纤溶酶原激活物抑制剂-1（PAI-1）]。在本综述中，我们将重点关注脂蛋白在血管壁中的病理生理功能。
