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国家卫生健康委员会
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英文作者:Wei Yifan Zhang Xianming Chen Zongyu Li Chunyu
单位:贵州医科大学附属医院呼吸与重症医学科,贵阳550004
英文单位:Department of Respiratory and Critical Care Medicine Affiliated Hospital of Guizhou Medical University Guiyang 550004 China
英文关键词:Ventilator-inducedlunginjury;Apoptosis;Autophagy;Ferroptosis;Pyroptosis
机械通气是急性呼吸衰竭的核心救治手段,但不合理使用易诱发机械通气相关性肺损伤(VILI),严重影响患者预后。程序性细胞死亡(PCD)的多种亚型在VILI病理进程中起关键调控作用:凋亡对肺组织细胞存活与纤维化呈双重调控效应;自噬作用具有异质性,依赖损伤模型等因素表现为保护或损伤效应;焦亡通过介导炎症因子释放加重损伤;铁死亡由机械牵拉诱导的氧化损伤与铁过载触发。各类PCD亚型间存在复杂交互调控网络,机械牵拉应激可能放大协同损伤效应。深入解析PCD调控网络,有望开发多维度靶向治疗方案,为VILI防治提供新突破。
Mechanical ventilation is the core treatment for acute respiratory failure, while inappropriate application tends to induce ventilator-induced lung injury (VILI), which seriously affects the prognosis of patients. Multiple subtypes of programmed cell death (PCD) play pivotal regulatory roles in the pathological process of VILI. Apoptosis exerts dual regulatory effects on pulmonary cell survival and fibrosis. Autophagy presents heterogeneous effects, playing protective or harmful roles depending on injury models and other factors. Pyroptosis aggravates lung injury by mediating the release of inflammatory factors. Ferroptosis is triggered by mechanical stretch-induced oxidative damage and iron overload. There exists a complex interactive regulatory network among various PCD subtypes, and mechanical stretch stress may amplify the synergistic damage effects. In-depth exploration of the PCD regulatory network is expected to facilitate the development of multi-dimensional targeted therapies and achieve new breakthroughs in the prevention and treatment of VILI.
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