斑块内泡沫细胞外迁功能障碍的研究进展  

Research progress of the dysfunction in foam cell emigration from plaques

作　　者：王中群[1] 李丽华[2] 严金川[1] 叶斐[1] 邵晨[1] WANG Zhong-Qun LI Li-Hua YAN Jin-Chuan YE Fei SHAO Chen(Department of Cardiology Department of Pathology, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu 212001, China)

机构地区：[1]江苏大学附属医院心内科,江苏省镇江市212001 [2]江苏大学附属医院病理科,江苏省镇江市212001

出　　处：《中国动脉硬化杂志》2017年第9期953-956,共4页Chinese Journal of Arteriosclerosis

基　　金：国家自然科学基金(81370408);江苏省自然科学基金(BK20131246);江苏省卫生厅项目(Q201308;QNRC2016836);镇江市社会发展项目(SH2015038;SH2015023);卫生部核医学重点实验室;江苏省分子核医学重点实验室开放课题(KF201504);江苏大学临床专项(JDLCZX001)

摘　　要：泡沫细胞的形成及外迁受抑是动脉壁斑块恶性重塑的关键环节,糖基化终末产物(AGE)则是糖尿病加速动脉粥样硬化进展的重要推手。基于国内外最新进展及本课题组已有成果,文章阐述了清道夫受体CD36在介导AGE关键活性成分羧甲基赖氨酸抑制泡沫细胞外迁中的作用及机制,希冀为今后靶向泡沫细胞外迁机制的治疗策略提供新的切入点。The formation and inhibited emigration of foam cells are the key events in malignant remodeling of artery plaques. Advanced glycation end products （AGE） play an important role in the course of diabetes-accelerating atheroscle- rotic progression. Based on the latest international research progress and our existing results, this paper elaborated the mechanism of CD36 modulating foam cell emigration from plaques inhibited by Ne-carboxymethyt-Lysine, which would pro- vide a new starting point for the treatment strategy of targeting foam cell migration mechanism in the future.

关 键 词：糖基化终末产物 清道夫受体 泡沫细胞 细胞迁移 动脉粥样硬化 

分 类 号：R363[医药卫生—病理学]