尾加压素Ⅱ与心肌纤维化关系的研究进展  

Research progress of relationship between Urotensin Ⅱ and myocardial fibrosis

作　　者：程兰[1] 黎连杰 杨絮[1] 张勇刚[1] CHENG Lan;LI Lian-Jie;YANG Xu;ZHANG Yong-Gang(Department of Cardiovascular Diseases, the Second Affiliated Hospital of Medical College, Shantou University, Shantou , Guangdong 515041, China)

机构地区：[1]汕头大学医学院附属第二医院心内科,广东省汕头市515041 [2]福州总医院神经外科,福建省福州市350025

出　　处：《中国动脉硬化杂志》2018年第5期521-524,共4页Chinese Journal of Arteriosclerosis

基　　金：国家自然科学基金面上项目(81270223)资助

摘　　要：尾加压素Ⅱ（urotensinⅡ,UⅡ）是一种强力缩血管活性肽,具有广泛的生物学功能。近年发现,在多种组织器官纤维化的过程中,UⅡ及其受体UT表达上调,参与了组织器官纤维化的发生发展。UⅡ参与心肌纤维化发生发展的机制十分复杂,涉及多个信号转导通路。文章重点就UⅡ与心肌纤维化的关系及其相关信号转导机制的研究进展做一简要综述。Urotensin Ⅱ is a kind of potent cyclic neuropeptide and has a series of biomedical functions. Recent studies have identified that the upregulation of urotensin Ⅱ and UT are involved in the process of organ fibrosis. The mechanisms of UⅡ effects are complicated and a number of signaling pathways activated by urotensin Ⅱ are related to myocardial fibrosis. This study reviewed the physiological and pathophysiological effects of urotensin Ⅱ involved in organ fibrosis,focusing on the correlation between urotensin Ⅱ and the concerned signaling pathways on myocardial fibrosis.

关 键 词：尾加压素Ⅱ 心肌纤维化 信号转导通路 

分 类 号：R5[医药卫生—内科学]