Martin-Ventura Jose L, Munoz-Garcia Begona, Egido Jesus, Blanco-Colio Luis M
Vascular Research Lab, Fundacion Jimenez Diaz, Autonoma University, Madrid, Spain.
Front Biosci. 2007 May 1;12:3656-67. doi: 10.2741/2342.
Cardiovascular diseases are the leading cause of mortality in the Western world. The underlying pathological process is a thickening of the arterial wall due to the formation of atheromatous plaques which contain a lipid core covered by a fibrous cap. The main mechanisms involved in atherogenesis are: lipoprotein retention, endothelial cell activation, vascular smooth muscle cell proliferation, macrophage infiltration, proteolytic injury, neovascularization and apoptosis. Different members of the tumor necrosis factor family (TNF) of proteins have been detected in human atherosclerotic plaques, among these are TNF-related apoptosis-inducing ligand (TRAIL) and its receptors (TRAIL-Rs and osteoprotegerin, OPG). In this review, the involvement of TRAIL and its receptors in the mechanisms underlying atherothrombosis is reviewed. In this respect, there are still some controversial data on the effects of TRAIL on inflammation and apoptosis of vascular cells. However, recent in vivo studies have suggested a potential proinflammatory and proapoptotic role of TRAIL in vascular injury. In addition, soluble forms of the TNF-superfamily can be released extracellularly and have been detected in human plasma. For this reason, we different studies evaluating the potential use of TRAIL and OPG plasma levels as markers of vascular injury are discussed.
心血管疾病是西方世界的主要死因。潜在的病理过程是动脉壁增厚，这是由于形成了含有脂质核心且被纤维帽覆盖的动脉粥样硬化斑块。动脉粥样硬化形成涉及的主要机制有：脂蛋白潴留、内皮细胞活化、血管平滑肌细胞增殖、巨噬细胞浸润、蛋白水解损伤、新生血管形成和细胞凋亡。在人类动脉粥样硬化斑块中已检测到肿瘤坏死因子家族（TNF）的不同成员，其中包括肿瘤坏死因子相关凋亡诱导配体（TRAIL）及其受体（TRAIL-Rs和骨保护素，OPG）。在本综述中，对TRAIL及其受体在动脉粥样硬化血栓形成机制中的作用进行了综述。在这方面，关于TRAIL对血管细胞炎症和凋亡的影响仍存在一些有争议的数据。然而，最近的体内研究表明TRAIL在血管损伤中具有潜在的促炎和促凋亡作用。此外，TNF超家族的可溶性形式可在细胞外释放，并已在人体血浆中检测到。因此，我们讨论了不同研究评估TRAIL和OPG血浆水平作为血管损伤标志物的潜在用途。
