线粒体改变与阻塞性呼吸睡眠暂停低通气综合征关系的研究进展  

Progress of study on changes of mitochondrial and its role in obstructive sleep apnea hypopnea syndrome

作　　者：刘嫣方[1] 林江[1] 付敏[1] 马吉春[1] 陈芹[1] 钱炜[2] 

机构地区：[1]镇江市第一人民医院中心实验室,江苏镇江212002 [2]镇江市第一人民医院耳鼻咽喉科

出　　处：《临床耳鼻咽喉头颈外科杂志》2016年第6期510-512,共3页Journal of Clinical Otorhinolaryngology Head And Neck Surgery

基　　金：江苏省卫生厅医学科研招标立项课题(No:H201353);镇江市第八批科技计划(科技基础设施)项目-镇江市干细胞应用研究重点实验室(No:SS2012003)

摘　　要：阻塞性呼吸睡眠暂停低通气综合征（obstructive sleep apnea hypopnea syndrome,OSAHS）是一种由反复的咽腔部分或完全塌陷引起的,以睡眠呼吸暂停、呼吸浅慢、血氧饱和度减低以及睡眠觉醒为特征的慢性疾病。该病从婴幼儿时期至老年任何年龄均可发病,且发病率与年龄和性别有明显的相关性。在西方国家成年男性和女性中的发病率已分别达到3%~7%和2%~5%,在儿童中的发病率为1%~3%。Obstructive sleep apnea hypopnea syndrome（OSAHS）is a common respiratory disease which has become an important public health problem.A high prevalence of OSAHS in the elderly may suggest that aging could be considered as a risk factor for the development of OSAHS.Recent work that has advanced understanding of mutations accumulating over time in the mitochondrial DNA（mtDNA）has been closely associated with aging.More and more researchers pay attention to changes of mitochondria morphology,electron transport chain enzymes and mtDNA.The process research of accumulation of circular mtDNA bearing deletions or mtDNA with accumulated point mutations in OSAHS subjects might be able to make mitochondrial become a representative biomarker for adverse outcomes from oxidative stress and cardiovascular diseases in the future.

关 键 词：睡眠呼吸暂停低通气综合征 阻塞性 衰老 线粒体 氧化应激 

分 类 号：R563.8[医药卫生—呼吸系统]