机械应力诱导心肌重构的研究进展

doi:10.12066/j.issn.1007-2861.2139

上海大学学报(自然科学版) ›› 2019, Vol. 25 ›› Issue (3): 375-380.doi: 10.12066/j.issn.1007-2861.2139

所属专题：精准与转化医学

机械应力诱导心肌重构的研究进展

吴剑, 邹云增()

复旦大学附属中山医院上海市心血管病研究所, 上海200032

收稿日期:2019-04-26 出版日期:2019-06-30 发布日期:2019-06-24
通讯作者: 邹云增 E-mail:zou.yunzeng@zs-hospital.sh.cn
作者简介:邹云增,教授,博士生导师,教育部长江学者特聘教授,国家自然科学基金杰出青年科学基金获得者,上海市领军人才。
复旦大学附属中山医院心内科, 教授, 博士生导师, 复旦大学附属中山医院临床医学研究院副院长, 上海市心血管病研究所副所长、中心实验室主任, 复旦大学生物医学研究院双聘教授. 1984 年7 月本科毕业于北京医学院医学系, 1997 年3 月获日本东京大学医学博士学位, 1997 年至2000 年在东京大学医学部循环器内科做博士后. 2004 年9 月人才引进到复旦大学附属中山医院心内科任教授至今. 2005 年被评为教育部长江学者特聘教授, 同年获国家自然科学基金杰出青年科学基金和上海市优秀学科带头人, 2013 年获上海市十大科技精英,2014 年获上海市领军人才, 2015 年获上海市侨界十杰. 主要研究方向是高血压心肌肥厚、心肌重构和心力衰竭, 先后承担了国家“十五”科技攻关课题1 项、国家“973”项目课题1 项、国家自然科学基金重点项目3 项、国家自然科学基金国际重大合作项目1 项等国家级课题. 以第一/共一和通信/共同通信作者在Nature Cell Biology, Circulation, Circulation Research,Hypertension, JBC 等杂志发表SCI 论文200 余篇, 授权国家专利2 项以第一完成人获中华医学科技进步三等奖、教育部科技奖二等奖和上海市科技进步一等奖. 兼任中国医师协会心力衰竭专委会副主委, 中华医学会心血管病学专委会基础学组副组长, 中国病理生理学会心血管专委会委员, 国际心脏研究会(ISHR)中国分会执委会委员、中国转化医学工作委员会副主委, 世界中医药学会联合会络病学分会副会长, 美国心脏协会Fellow(FAHA), 欧洲心脏学会Fellow(FESC),《中华心肌病与心力衰竭杂志》副总编,《临床心血管病杂志》副主编,《中华心血管病学杂志》、《中国分子心脏病杂志》、《上海医学》等杂志编委.
基金资助:
国家自然科学基金资助项目(31430039);国家自然科学基金资助项目(81670228);国家自然科学基金资助项目(81730009);上海市科委实验动物研究专项资助项目(16140901100);上海市卫计委科研课题面上资助项目(201640044);复旦大学附属中山医院人才培养计划资助项目(2017ZSYXQN09)

Recent progress in understanding mechanical stretch induced myocardial remodeling

WU Jian,ZOU Yunzeng()

Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University,Shanghai 200032, China

Received:2019-04-26 Online:2019-06-30 Published:2019-06-24
Contact: Yunzeng ZOU E-mail:zou.yunzeng@zs-hospital.sh.cn

摘要/Abstract

摘要：

心肌重构是心力衰竭等心血管主要事件的独立危险因素. 血流动力学病理性改变产生的机械应力异常增加可直接触发心肌重构, 同时伴随神经体液因子表达升高, 产生协同作用,进一步加重心肌重构. 根据机械应力超负荷不同, 心肌重构可分为压力超负荷心肌重构和容量超负荷心肌重构. 两类心肌重构在心脏大体结构、细胞和分子水平上存在明显差异. 虽然容量超负荷在心脏疾病中普遍存在, 但既往研究多集中于压力超负荷心肌重构, 而对容量超负荷心肌重构认识不足. 近期发现钙处理蛋白(如钙/钙调素依赖蛋白激酶Ⅱ)和蛋白激酶B(Akt)可能介导两类超负荷心肌重构的差异. 整合已有报道及本课题组的最新成果, 概述两类机械应力心肌重构的异同, 为心肌肥厚的精准化研究和个性化诊疗提供参考.

关键词: 心肌重构, 压力超负荷, 容量超负荷, 向心性, 离心性

Abstract:

Myocardial remodeling is an independent risk factor for major cardiovascular events such as heart failure. An abnormal increase in mechanical stress caused by hemodynamic pathological changes can directly trigger myocardial remodeling, accompanied by increased expression of neurohumoral factors, resulting in a synergistic effect which could further aggravate myocardial remodeling. Myocardial remodeling can be divided into pressure overload myocardial remodeling and volume overload myocardial remodeling, according to the type of mechanical stress overload. There are significant differences in the two types of myocardial remodeling at the gross structural, cellular, and molecular levels of the heart. Although volume overload is prevalent in various heart diseases, previous studies have focused on pressure overload myocardial remodeling, with a lack of sufficient elucidation of volume overload myocardial remodeling. It has been discovered through research that calcium-handling proteins and Akt may be held responsible for the difference between the two types of overload myocardial remodeling. This paper, which combines the previous achievements with our latest research results, outlines the similarities and differences between the two types of mechanical stress myocardial remodeling, attempts to shed some new light on precision research and personalized diagnosis and treatment of cardiac hypertrophy.

Key words: myocardial remodeling, pressure overload, volume overload, concentric, eccentric

中图分类号:

R541

吴剑, 邹云增. 机械应力诱导心肌重构的研究进展[J]. 上海大学学报(自然科学版), 2019, 25(3): 375-380.

WU Jian , ZOU Yunzeng . Recent progress in understanding mechanical stretch induced myocardial remodeling[J]. Journal of Shanghai University（Natural Science Edition）, 2019, 25(3): 375-380.

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机械应力诱导心肌重构的研究进展

Recent progress in understanding mechanical stretch induced myocardial remodeling

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