转录活化因子3调控肺泡巨噬细胞在急性呼吸窘迫综合征中作用的研究进展

Research progress of transcription activating factor 3 in regulating the alveolar macrophages in acute respiratory distress syndrome

急性呼吸窘迫综合征(ARDS)是由感染、创伤等多种肺内和(或)肺外因素导致的急性弥漫性肺损伤,失控的炎症反应是其主要病理特征;而肺泡巨噬细胞极化状态对ARDS炎症反应可产生不同的影响。转录活化因子3(ATF3)是细胞应激早期一种快反应基因,近年来发现其通过调控肺泡巨噬细胞功能,对ARDS炎症反应有重要调节作用。现围绕ATF3对肺泡巨噬细胞极化、细胞自噬以及内质网应激(ERS)的调控作用及其对ARDS炎症进程的影响进行综述,为ARDS的防治提供新的研究方向。

Acute respiratory distress syndrome(ARDS)refers to acute diffuse lung injury caused by a variety of intrapulmonary and/or extrapulmonary factors such as infection and trauma.Uncontrolled inflammatory response is the main pathological feature.Different functional states of alveolar macrophages have different effects on inflammatory response.Transcription activating factor 3(ATF3)is a fast response gene in the early stage of stress.In recent years,it has been found that ATF3 plays an important role in regulating the inflammatory response of ARDS by regulating the function of macrophages.This paper reviews the regulatory effects of ATF3 on alveolar macrophage polarization,autophagy and endoplasmic reticulum stress and its effects on the inflammatory process of ARDS,aiming to provide a new research direction for the prevention and treatment of ARDS.