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白介素-33在急性呼吸窘迫综合征中的研究进展

发布时间:2017-12-30 21:57

  本文关键词:白介素-33在急性呼吸窘迫综合征中的研究进展 出处:《重庆医科大学学报》2016年04期  论文类型:期刊论文


  更多相关文章: 急性呼吸窘迫综合症 白介素- 细胞因子 警报素 信号通路


【摘要】:急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)是以顽固性低氧血症和进行性呼吸困难为主要临床特点的综合征,是危重症患者死亡的主要原因之一。尽管,近年来医疗技术的迅猛发展和新的药物的应用使ARDS的预后有所改善,但其病死率仍高达40%~50%。因此,更充分的了解ARDS的发病机制,实现早期诊断,为临床上ARDS的防治提供指导仍是呼吸和重症医学界研究的重点和热点。白介素(interleukin,IL)-33是新近发现的IL-1家族成员,在炎症、感染、自身免疫性疾病等多种疾病中发挥重要的警报素作用,促进机体的炎症反应,加重机体组织的损伤。故IL-33及其信号通路可能成为阻断炎症通路的级联反应的一个潜在的分子靶点。本文就IL-33在ARDS中的研究进展做一综述。
[Abstract]:Acute respiratory distress syndrome. ARDS is a syndrome characterized by intractable hypoxemia and progressive dyspnea, and is one of the leading causes of death in critically ill patients. In recent years, with the rapid development of medical technology and the application of new drugs, the prognosis of ARDS has been improved, but its mortality is still as high as 40%. Therefore, the pathogenesis of ARDS is fully understood. To achieve early diagnosis and provide guidance for the prevention and treatment of ARDS in clinic is still the focus and focus of the research of respiratory and critical medicine. IL)-33 is a newly discovered member of IL-1 family, which plays an important role in many diseases, such as inflammation, infection, autoimmune diseases and so on. Therefore, IL-33 and its signaling pathway may become a potential molecular target for blocking the cascade of inflammatory pathways. This paper reviews the progress of IL-33 in ARDS. State.
【作者单位】: 重庆医科大学附属第一医院急诊医学科和重症医学科;
【基金】:国家自然科学基金资助项目(编号:81570069)
【分类号】:R563.8
【正文快照】: 白介素(interleukin,IL)-33是IL-1家族的新成员,在正常人体组织中持续表达[1-2],具有核内调控基因转录和核外调节炎症反应的双重功能[3-4]。目前,IL-33作为炎症细胞因子的作用及其作用机制越来越受到重视,本文就IL-33在ARDS这一以炎症反应为中心环节的临床综合征中的研究进展

本文编号:1356679

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