铁死亡及其在肺部疾病中的作用

Ferroptosis and its role in pulmonary disease

铁死亡为一种新发现的细胞程序性死亡方式,其发生机制复杂。铁过载、脂质过氧化、谷胱甘肽耗竭和丙二醛累积可通过调节细胞内长链非编码RNA、Xc-系统、GPX4、肿瘤抑制因子和核因子E2相关因子的表达诱导铁死亡。越来越多的研究表明,铁死亡与肺血管重构、急性肺损伤、慢性阻塞性肺疾病、特发性肺纤维化、肺部感染、支气管哮喘等密切相关。

Ferroptosis,as a newly discovered form of programmed cell death,has complex pathogenesis.Iron overload,lipid peroxidation,glutathione depletion and malondialdehyde accumulation are capable of inducing ferroptosis by regulating the expression of intracellular long non-coding RNAs,system Xc-,GPX4,tumor suppressor factors,and nuclear factor erythroid 2 related factor.In increasing studies ferroptosis plays an important role in pulmonary vascular remodeling,acute lung injury,chronic obstructive pulmonary disease,idiopathic pulmonary fibrosis,pulmonary infection,bronchial asthma.