非血脂因素致血管内皮损伤时黏附分子变化的研究进展

随着社会老龄化的加快,动脉粥样硬化的发生率逐年升高。目前认为动脉粥样硬化的始动环节是血管内皮损伤,而脂质代谢异常是血管损伤的主要危险因素。现研究发现一些非脂质物质在血管损伤机制中起着重要的作用,如高同型半胱氨酸、高血糖以及高尿酸等。这些非脂质因素主要作用于血管内皮细胞,通过干扰黏附分子的表达、改变内皮细胞的病理生理状态,进而导致血管内皮的损伤,促进动脉粥样硬化病灶的形成。本文主要介绍非脂质危险因素致内皮损伤时细胞黏附分子的变化的一些作用机制,并介绍干预黏附分子表达的一些治疗靶点,对治疗动脉粥样硬化所导致的冠心病、心肌梗塞等心血管疾病具有重要的临床意义。

Progress in the changes of adhesion molecules in non-lipid factors induced atherosclerotic vascular endothelial injury

With the accelerated aging of society, the incidence of atherosclerosis(As) is increasing year by year. Now that the initial event of the atherosclerosis is endothelial damage, while lipid metabolism is a major risk factor for vascular injury. But now research shows that some non-lipid material also play an important role in the development of As, such as high homocysteine (HHCy), high blood sugar and high uric acid. These non-lipid factors play a major role in vascular endothelial cells, interference by expression of sticky molecule, changing the state of the pathophysiology of endothelial cells, leading to endothelial damage, contributing to the formation of As lesions. This paper describes some of the mechanisms that the changes of adhesion molecules in non-lipid factors induced atherosclerotic vascular endothelial injury, and describes some of the therapeutic intervention targets expression of adhesion molecules, which has important clinical significance for the treatment of atherosclerosis leading to coronary heart disease, myocardial infarction and other cardiovascular diseases.