细胞程序性坏死在急性肺损伤中作用的研究进展

 程序性坏死作为一种新的细胞程序性死亡方式参与急性肺损伤（acute lung injury，ALI）的病理过程，主要在疾病前期由各类高危因素触发，由受体相互作用蛋白激酶1（receptor-interacting protein kinase 1，RIPK1）、RIPK3、混合谱系激酶结构域样蛋白（mixed-lineage kinase domain-like protein，MLKL）介导，导致肺泡上皮细胞、血管内皮细胞、肺泡巨噬细胞等细胞死亡，直接或通过调节机体炎症反应造成严重的肺泡结构损伤及肺水肿，应用抑制剂阻断程序性坏死可以减轻肺损伤。本文就程序性坏死在ALI中的作用进行综述，以期为临床筛选高危患者和治疗提供依据。

Research progresses on the role of necroptosis in acute lung injury

A newly reported programmed cell death, necroptosis,is involved in the pathological process of acute lung injury (ALI).Necroptosis is triggered in early stage of the disease under several high risk factors and mainly mediated by receptor interacting protein kinase 1 (RIPK1),RIPK3,and mixed lineage kinase domain-like proteins (MLKL).Necroptosis of alveolar epithelial cells,vascular endothelial cells,alveolar macrophages and other cells causes severe alveolar injury and edema directly or by regulating inflammatory response.The application of inhibitors to block necroptosis can reduce lung injury.This review summarizes the role of necroptosis in ALI to provide information to screen high-risk patients and therapy.