急性肺损伤中细胞铁死亡与线粒体自噬的关系：一篇综述
Relationship between ferroptosis and mitophagy in acute lung injury: a mini-review.
作者信息
Cheng Yunhua, Zhu Liling, Xie Shuangxiong, Lu Binyuan, Du Xiaoyu, Ding Guanjiang, Wang Yan, Ma Linchong, Li Qingxin
机构信息
The First School of Clinical Medicine of Gansu University of Chinese Medicine, Gansu University of Chinese Medicine, Lanzhou, Gansu Province, China.
Department of Thoracic Surgery, The 940th Hospital of Joint Logistics Support Force of Chinese People's Liberation Army, Lanzhou, Gansu Province, China.
出版信息
PeerJ. 2024 Sep 10;12:e18062. doi: 10.7717/peerj.18062. eCollection 2024.
Acute lung injury (ALI) is one of the most deadly and prevalent diseases in the intensive care unit. Ferroptosis and mitophagy are pathological mechanisms of ALI. Ferroptosis aggravates ALI, whereas mitophagy regulates ALI. Ferroptosis and mitophagy are both closely related to reactive oxygen species (ROS). Mitophagy can regulate ferroptosis, but the specific relationship between ferroptosis and mitophagy is still unclear. This study summarizes previous research findings on ferroptosis and mitophagy, revealing their involvement in ALI. Examining the functions of mTOR and NLPR3 helps clarify the connection between ferroptosis and mitophagy in ALI, with the goal of establishing a theoretical foundation for potential therapeutic approaches in the future management of ALI.
急性肺损伤（ALI）是重症监护病房中最致命且常见的疾病之一。铁死亡和线粒体自噬是ALI的病理机制。铁死亡会加重ALI，而线粒体自噬则对ALI起调节作用。铁死亡和线粒体自噬均与活性氧（ROS）密切相关。线粒体自噬可调节铁死亡，但铁死亡与线粒体自噬之间的具体关系仍不清楚。本研究总结了以往关于铁死亡和线粒体自噬的研究结果，揭示了它们在ALI中的作用。研究mTOR和NLPR3的功能有助于阐明ALI中铁死亡与线粒体自噬之间的联系，旨在为未来ALI治疗方法的潜在治疗途径奠定理论基础。
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