呼吸重叠综合征患者中性粒细胞凋亡机制的研究进展  

Research Progress of Neutrophil Apoptosis Mechanism in Patients with Respiratory Overlap Syndrome

作　　者：李鑫[1] 曹洁[1] LI Xin;CAO Jie(Department of Respiratory and Critical Care Medicine,Tianjin Medical University General Hospital,Tianjin 300052,China)

机构地区：[1]天津医科大学总医院呼吸与危重症医学科,天津300052

出　　处：《医学综述》2021年第11期2216-2221,共6页Medical Recapitulate

基　　金：国家自然科学基金(81670084)。

摘　　要：慢性阻塞性肺疾病(COPD)与阻塞性睡眠呼吸暂停(OSA)是临床最常见的两种呼吸系统疾病,当COPD与OSA并存时称为呼吸重叠综合征(OS)。与单纯患有COPD或OSA的患者相比,OS患者的心血管疾病发病率更高,损害也更严重。血管内皮细胞功能受损与心血管疾病关系密切,而多形核中性粒细胞(PMN)凋亡延迟是内皮细胞损伤过程中的关键环节。低氧情况下,PMN凋亡延迟可导致炎症因子和活性氧类释放增加,引起内皮细胞损伤和严重的心血管功能障碍。因此,了解OS患者低氧情况下PMN凋亡机制对减少心血管损害至关重要。未来可通过干预PMN的异常凋亡,为OS患者心血管损害的治疗提供新靶点。Chronic obstructive pulmonary disease(COPD)and obstructive sleep apnea(OSA)are two common chronic respiratory diseases that often coexist in individuals and are known as respiratory overlap syndrome(OS).The patients with OS have a higher incidence of cardiovascular disease and more severe impairment than patients with COPD or OSA alone.The damage of endothelial cell function is closely related to cardiovascular disease,and the delay of polymorphonuclear neutrophil(PMN)apoptosis is closely related to delayed apoptosis of PMN in hypoxic conditions can lead to increased release of inflammatory factors and reactive oxygen species,resulting in endothelial cell injury and severe cardiovascular dysfunction.Therefore,understanding the mechanism of PMN apoptosis in OS patients is crucial to reduce the cardiovascular damage.In the future,it can provide a new target for the treatment of cardiovascular damage in OS patients by intervening in abnormal PMN apoptosis.

关 键 词：呼吸重叠综合征 多形核中性粒细胞 凋亡 低氧 

分 类 号：R563.9[医药卫生—呼吸系统]