半乳糖凝集素-3致心肌纤维化机制的研究进展  

The mechanism of galectin-3 in myocardial fibrosis

作　　者：李问渠 覃小娟 张丽[1,2] 韩正阳 谢明星[1,2] LI Wenqu;QIN Xiaojuan;ZHANG Li;HAN Zhengyang;XIE Mingxing(Department of Ultrasoud,Union Hospital of Tongji Medical College,Huazhong University of Science and Technology,Wuhan,430022,China;Hubei Province Key Laboratory of Molecular Imaging,Union Hospital of Tongji Medical College,Huazhong University of Science and Technology,Wuhan,430022,China)

机构地区：[1]华中科技大学同济医学院附属协和医院超声影像科,武汉430022 [2]华中科技大学同济医学院附属协和医院分子影像湖北省重点实验室,武汉430022

出　　处：《临床心血管病杂志》2020年第12期1079-1082,共4页Journal of Clinical Cardiology

基　　金：国家自然科学基金(No:81901769)。

摘　　要：半乳糖凝集素-3(Gal-3)是一种通过识别β-糖苷介导多种细胞间相互作用的凝集素,参与纤维化、炎症、自身免疫反应、肿瘤等病理过程。Gal-3与心肌纤维化的发生发展密切相关,可以作为心力衰竭的独立预测因子。本文主要对Gal-3致心肌纤维化机制的最新研究进展进行综述,同时进一步讨论Gal-3作为抗心肌纤维化治疗新靶点的可能性。Galectin-3(Gal-3)is a lectin that mediates a variety of cellular interactions through the recognition ofβ-glycoside,and the protein is involved in many pathological processes such as fibrosis,inflammation,autoimmunity,and tumor.Gal-3 is closely related to the development of myocardial fibrosis and can be used as an independent predictor of heart failure.This article systematically reviews the mechanism of Gal-3 in myocardial fibrosis,and discusses the therapeutic potential of Gal-3 on myocardial fibrosis.

关 键 词：半乳糖凝集素-3 心肌纤维化 心力衰竭 

分 类 号：R542.2[医药卫生—心血管疾病]