非血脂因素致血管内皮损伤时黏附分子变化的研究进展

发布时间：2018-12-30 22:10

【摘要】：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。
[Abstract]:With the aging of society, the incidence of atherosclerosis increases year by year. At present, it is believed that vascular endothelial injury is the initiation of atherosclerosis, and abnormal lipid metabolism is the main risk factor of vascular injury. Some non-lipid substances have been found to play an important role in vascular injury, such as homocysteine, hyperglycemia and hyperuric acid. These non-lipid factors mainly act on vascular endothelial cells. By interfering with the expression of adhesion molecules, the pathophysiological state of endothelial cells is changed, which leads to the injury of vascular endothelium and promotes the formation of atherosclerotic lesions. This paper mainly introduces the mechanism of cell adhesion molecule changes in endothelial injury induced by non-lipid risk factors, and some therapeutic targets for the treatment of coronary heart disease caused by atherosclerosis. Cardiovascular diseases such as myocardial infarction have important clinical significance.
【作者单位】： 济南大学山东省医学科学院医学与生命科学学院;济南大学山东省医学科学院药物研究所山东省罕少见病重点实验室;
【基金】：山东省自主创新及成果转化专项(201402103)
【分类号】：R543.5

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