PM2.5诱导基因甲基化水平改变在先天性心脏畸形形成中的机制  

Mechanism of Methylation Change Caused by PM2.5 in Congenital Heart Defects

作　　者：庄子萌 蒋叶香 阿迪拉·阿里木 张珺媛 蒋沐岐 宋耿 梁华敏[1] 王维[1] 朱敏洁[1] Zhuang Zimeng;Jiang Yexiang;Alim Adila(Department of Physiology,Basic Medical College,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China)

机构地区：[1]华中科技大学同济医学院基础医学院生理学系,武汉430030

出　　处：《华中科技大学学报（医学版）》2020年第6期766-769,共4页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong

基　　金：国家自然科学基金资助项目(No.81971218)。

摘　　要：细颗粒物PM2.5作为雾霾的重要组成成分是近年来环境卫生研究的热点,PM2.5是多种先天性心脏畸形的危险因素之一,但目前对于PM2.5导致先天性心脏畸形的毒性机制并不明确。先天性心脏畸形与某些基因甲基化水平改变有关,而PM2.5可影响DNA甲基化,该文从甲基化水平改变的角度对PM2.5暴露与先天性心脏畸形的关系进行综述,并展望了甲基化水平改变在PM2.5致病机制研究中的应用。As an important composition of smog,fine particulate matter(PM2.5)is a research hotspot in recent study of environmental health.PM2.5 is a risk factor of several congenital heart defects but the toxicant mechanisms of PM2.5 remain uncertain.Congenital heart defects are relevant to methylation change of some genes while DNA methylation can be influenced by PM2.5.This review discusses the relationship between PM2.5 exposure with congenital heart defects in the view of methylation change,and the prospect of the application of methylation change in the mechanism study of PM2.5.

关 键 词：先天性心脏畸形 细颗粒物 甲基化 

分 类 号：R541.1[医药卫生—心血管疾病]