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铁死亡在中枢神经系统损伤疾病中的作用。

The role of ferroptosis in central nervous system damage diseases.

作者信息

Li Mingzhu, Jin Shengbo, Zhu Xudong, Xu Jian, Cao Yang, Piao Haozhe

机构信息

Department of Integrated Traditional Chinese and Western Medicine Medical Oncology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang, Liaoning Province, China.

College of Acupuncture and Massage of Liaoning Chinese Traditional Medicine, Shenyang, Liaoning Province, China.

出版信息

PeerJ. 2024 Jan 30;12:e16741. doi: 10.7717/peerj.16741. eCollection 2024.

Abstract

Ferroptosis is a form of cell death, , programmed cell death characterized by lipid peroxidation and iron dependence, which has unique morphological and biochemical properties. This unique mode of cell death is driven by iron-dependent phospholipid peroxidation and regulated by multiple cell metabolic pathways, including redox homeostasis, iron metabolism, mitochondrial activity, and the metabolism of amino acids, lipids, and sugars. Many organ injuries and degenerative pathologies are caused by ferroptosis. Ferroptosis is closely related to central nervous system injury diseases and is currently an important topic of research globally. This research examined the relationships between ferroptosis and the occurrence and treatment of central nervous system injury diseases. Additionally, ferroptosis was assessed from the aspect of theory proposal, mechanism of action, and related signaling pathways per recent research. This review provides a relevant theoretical basis for further research on this theory, the prospect of its development, and the prevention and treatment of such diseases.

摘要

铁死亡是一种细胞死亡形式,即程序性细胞死亡,其特征在于脂质过氧化和铁依赖性,具有独特的形态学和生化特性。这种独特的细胞死亡模式由铁依赖性磷脂过氧化驱动,并受多种细胞代谢途径调节,包括氧化还原稳态、铁代谢、线粒体活性以及氨基酸、脂质和糖类的代谢。许多器官损伤和退行性病变都是由铁死亡引起的。铁死亡与中枢神经系统损伤疾病密切相关,是目前全球重要的研究课题。本研究探讨了铁死亡与中枢神经系统损伤疾病发生及治疗之间的关系。此外,根据最近的研究,从理论提出、作用机制和相关信号通路等方面对铁死亡进行了评估。本综述为进一步研究该理论、其发展前景以及此类疾病的预防和治疗提供了相关理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc1b/10836208/625830be18d5/peerj-12-16741-g001.jpg

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