CD163在糖尿病性冠状动脉粥样硬化中的作用及机制  

The Action and Mechanism of CD163 in Diabetic Coronary Atherosclerosis

作　　者：王玉泉[1] 吕湛[1] 

机构地区：[1]川北医学院附属医院心血管内科,四川省南充市637000

出　　处：《中国动脉硬化杂志》2013年第2期187-192,共6页Chinese Journal of Arteriosclerosis

摘　　要：糖尿病是冠心病的等危症,糖尿病致冠状动脉粥样硬化机制复杂,初始原因为长期的血糖浓度升高,高血糖可通过短期反复的细胞内外信号通路活性及代谢的改变而导致内皮细胞的持久损伤,从而促进动脉粥样硬化的发生。研究显示,在高血糖致内皮细胞损伤进而导致动脉粥样硬化的具体机制中,慢性炎症和氧化应激程度增加被认为是最主要的病理生理因素和各种机制的共同通路。近年来研究发现,血红蛋白清道夫受体(CD163)具有明显的抗炎和抗脂质过氧化作用,在糖尿病致冠状动脉粥样硬化的防御体系中起重要作用。Diabetes mellitus is a risk equivalent of coronary heart disease and the pathogenesis of diabetic coronary atherosclerosis （As） is complicated, long-term hyperglycemia is recognized as the primary culprit for it can damage the endothelial cells persistently through interfering the intracellular signaling pathway and metabolism. Researches show that the increase of chronic inflammation and excessive oxidative stress is the most important pathophysiologic mechanisms for As and the common pathway of pathogenesis under the circumstance of hyperglycemia. In recent years, the study found that the hemoglobin scavenger receptor （CD163） has an obvious anti-inflammatory and anti-lipid peroxidation capacity and may play an important role in the prevention of diabetic coronary As.

关 键 词：CD163 糖尿病性冠状动脉粥样硬化 慢性炎症 氧化应激 

分 类 号：R541.4[医药卫生—心血管疾病]