摘要
特发性肺纤维化(IPF)作为一种进行性、致死性的间质性肺疾病,病因至今尚未明确,病理表现为持续肺损伤导致的异常修复改变.巨噬细胞在IPF发病机制中发挥着关键作用.在不同的局部微环境中,巨噬细胞可表现出经典活化(M1)或交替活化(M2)的表型.M1扮演促进炎症反应的关键角色,参与引起肺泡组织损伤的过程;而M2参与伤口愈合以及终止肺部炎症反应.先前的研究表明,肺纤维化中5-羟色胺(5-HT)信号激活增强,5-HT受体在促纤维化作用中发挥重要作用.5-HT作为一种多功能的信号分子,与肺巨噬细胞极化、早期肺组织损伤、异常增殖修复以及晚期细胞外基质(ECM)沉积密切相关.本文就5-HT与M2巨噬细胞在IPF发病中的作用以及5-HT可能的调控机制进行综述,以期为进一步深入研究提供参考.
Idiopathic pulmonary fibrosis(IPF)is a progressive and fatal interstitial lung disease,the cause is not yet clear.Pathological manifestations are abnormal repair changes resulting from sustained lung injury.Macrophages have been identified as playing a key role in IPF pathogenesis.In different local microenvironments,macrophages can exhibit either classically activated(M1)or alternately activated(M2)phenotypes.M1 plays a key role in promoting inflammatory response and is involved in the process of causing alveolar tissue injury.M2 is involved in wound healing and stopping lung inflammation.Previous studies have shown that activation of 5-hydroxytryptamine(5-HT)signaling is enhanced in pulmonary fibrosis and that 5-HT receptors play an important role in the observed pro-fibrotic effects.As a multifunctional signaling molecule,5-HT is closely related to lung macrophage polarization,early lung tissue injury,abnormal proliferation and repair,and late extracellular matrix(ECM)deposition.This article reviewed the role of 5-HT and M2 macrophages in the pathogenesis of IPF and the possible regulatory mechanism of 5-HT,in order to provide a reference for further research.
作者
邓一鸣
邓常文
朱晓萍
Deng Yiming;Deng Changwen;Zhu Xiaoping(Department of Respiratory and Critical Care Medicine,East Hospital,Tongji University,Shanghai 200120,China)
出处
《中华危重病急救医学》
CAS
CSCD
北大核心
2023年第9期1004-1008,共5页
Chinese Critical Care Medicine
基金
国家自然科学基金项目(81970089)。
