摘要
肺纤维化是一种间质性肺疾病,其临床表现为进行性的呼吸困难.由于当前治疗手段有限,患者最终常因呼吸衰竭而死亡.肺纤维化的发生机制目前尚未明确.铁死亡是一种非凋亡性、铁依赖性的细胞死亡模式.本文从谷胱甘肽过氧化物酶 4(GPX4)与铁死亡抑制蛋白(FSP1)、活性氧(ROS)、衰老、内质网应激等角度,探讨铁死亡调控肺纤维化的可能机制,以期为治疗提供更多的研究靶点和方向.
Abstract
Pulmonary fibrosis is an interstitial pneumonia,characterized by progressive respiratory difficulty.Due to limited current therapeutic options,patients may finally die of respiratory failure.The mechanisms underlying the development of pulmonary fibrosis are not fully understood.Ferroptosis is a non-apoptotic,iron-dependent form of cell death.In this paper,we explores the potential mechanisms by which ferroptosis regulates pulmonary fibrosis,from the perspectives of glutathione peroxidase 4(GPX4)and ferroptosis-suppressing protein(FSP1),reactive oxygen species(ROS),aging,and endoplasmic reticulum stress,in order to provide more research targets and directions for treatment.
基金项目
国家自然科学基金青年基金(82104624)
江苏省高等学校自然科学研究面上项目(21KJB320003)
江苏省高等学校大学生创新创业训练计划重点项目(202210313048Z)
NETL
NSTL
维普
万方数据