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心力衰竭时高迁移率族蛋白(HMG)B1和可溶性晚期糖基化终产物受体(sRAGE)的变化
引用本文:敖文杰,邹卓璇综述,张瑞英审校. 心力衰竭时高迁移率族蛋白(HMG)B1和可溶性晚期糖基化终产物受体(sRAGE)的变化[J]. 心脏杂志, 2017, 29(3): 356-360. DOI: 10.13191/j.chj.2017.0091
作者姓名:敖文杰  邹卓璇综述  张瑞英审校
作者单位:哈尔滨医科大学附属第一医院心内三科, 黑龙江 哈尔滨 150001
基金项目:黑龙江省教育厅科学技术研究项目资助(12541291)
摘    要:心力衰竭(HF)是多种心脏疾病的终末阶段,也是一种慢性炎症性疾病。高迁移率族蛋白(HMG)B1是机体非特异性炎症反应的敏感标志物,胞外的HMGB1通过与其高亲和力受体晚期糖基化终产物受体(RAGE)结合后参与心血管疾病的发生发展,而可溶性RAGE(sRAGE)可竞争性抑制全长RAGE的生物学效应,竞争结合HMGB1,从而减轻甚至抑制炎症反应,延缓HF的发生和发展,现就近年来研究发现的HMGB1、sRAGE在心血管疾病中所起的作用及其在治疗方面的进展做一综述。

关 键 词:高迁移率族蛋白B1   可溶性晚期糖基化终产物受体   心力衰竭
收稿时间:2015-10-21

Changes of high mobility protein B1 and soluble advanced glycation end product receptor in heart failure
Affiliation:Third Department of Cardiology, First Affiliated Hospital, Harbin Medical University, Harbin 150001, Heilongjiang, China
Abstract:Heart failure is considered to be a chronic inflammatory disease. High mobility group protein B1(HMGB1) is a sensitive marker of the body's nonspecific inflammation. Extracellular HMGB1 through its high affinity combined with receptor advanced glycation end product receptor(RAGE) participates in the occurrence of cardiovascular disease development. sRAGE can competitively inhibit RAGE biological effect and competitively combine with HMGB1 to reduce and inhibit inflammation, thus delaying the occurrence and development of heart failure. This article summarizes the recent progress in the role of HMGB1 and sRAGE in the development and treatment of cardiovascular disease.
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