氧化应激致组蛋白修饰在慢性阻塞性肺病发生发展中的作用  

The role of oxidative stress induced histone modification in chronic obstructive pulmonary disease

作　　者：孔令雯[1] 董竞成[1] 

机构地区：[1]复旦大学附属华山医院中西医结合科,上海医学博士研究生200040

出　　处：《医学研究生学报》2014年第9期968-972,共5页Journal of Medical Postgraduates

基　　金：国家重点基础研究发展计划(973计划)(2009CB523001);国家自然科学基金(81173390)

摘　　要：慢性阻塞性肺病(chronic obstructive pulmonary disease,COPD)是一种严重影响人类健康的疾病,目前为止发病机制尚不清楚。吸烟导致的肺组织氧化应激和慢性炎症是2个明确致病因素,以往氧化应激等环境因素和遗传因素在COPD发病中被认为是相互独立的危险因素,但是表观遗传学(epigenetic)的出现,把遗传和环境这2个独立的因素紧密地结合在一起。文中综述了COPD发病过程中,氧化应激所致的组蛋白修饰与COPD的肺部炎症、抗氧化反应、细胞凋亡、自噬及T细胞亚群的分化等病理改变的联系,揭示了表观遗传修饰在COPD发病中的重要地位,为该病的临床治疗提供更多的选择。Chronic obstructive pulmonary disease （ COPD） is a prevalent disease which is the fourth leading cause of death worldwide and will be the major economic burden of diseases according to the World Bank /World Health Organization .However , the pathogenesis of COPD is inadequately understood , oxidative stress and chronic inflammation are considered to be two independent path -ogenetic factors , but the epigenetic put them together because of changes of the environment lead to gene abnormal expression .This ar-ticle summarizes the relationship between histone modifications of genes induced by oxidative stress and the inflammation , antioxidant response, apoptosis, autophagy and the differentiation of T cell subsets in the pathogenesis of COPD .The work will provide more choices for clinical treatment of COPD .

关 键 词：组蛋白 慢性阻塞性肺病 氧化应激 组蛋白去乙酰化酶 去乙酰化酶1 

分 类 号：R563[医药卫生—呼吸系统]