激素抵抗型哮喘发病机制的研究进展  

Research progress on the pathogenesis of steroid resistant asthma

作　　者：朱桂萍(综述) 叶伶[1] 金美玲(审校)[1] ZHU Gui-ping;YE Ling;JIN Mei-ling(Department of Pulmonary and Critical Care Medicine,Zhongshan Hospital,Fudan University,Shanghai 200032,China)

机构地区：[1]复旦大学附属中山医院呼吸与危重症医学科,上海200032

出　　处：《复旦学报（医学版）》2021年第5期680-684,共5页Fudan University Journal of Medical Sciences

基　　金：国家重点研发计划(2017YFC0910003)。

摘　　要：激素抵抗型哮喘治疗困难,一直是哮喘研究的重点和难点。研究发现糖皮质激素受体(glucocorticoid receptor,GR)异常、组蛋白去乙酰化酶2(histone deacetylase,HDAC2)活性降低等经典机制在激素抵抗型哮喘发病中起重要作用。此外,Th细胞免疫失衡、感染、肥胖及非编码RNA、细胞自噬等因素在激素抵抗型哮喘中的作用也是近年研究的热点。本文对以上激素抵抗型哮喘发病机制的研究进展予以综述,以提高对激素抵抗型哮喘的认识,为未来的治疗提供方向。The difficulty in the treatment of steriod resistant asthma has always been the priority of asthma research.It has been found that abnormal glucocorticoid receptor(GR)and decreased histone deacetylase 2(HDAC2)activity play important roles in the pathogenesis of steroid resistant asthma.In addition,Th cell immune imbalance,infection,obesity,non-coding RNA and autophagy also play critical parts in steriod resistant asthma,becoming research focus in asthma recently.In this paper,the research progress of the pathogenesis of steriod resistant asthma above is reviewed in order to improve the understanding of steriod resistant asthma and provide directions for future treatment.

关 键 词：激素抵抗型哮喘 糖皮质激素受体(GR) 组蛋白去乙酰化酶2(HDAC2) TH1 TH17 感染 肥胖 

分 类 号：R562.25[医药卫生—呼吸系统]