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铁蛋白自噬和铁死亡在脑缺血再灌注损伤中的作用。

Ferritinophagy and Ferroptosis in Cerebral Ischemia Reperfusion Injury.

机构信息

School of Acupuncture-moxibustion, Tuina and Rehabilitation, Hunan University of Chinese Medicine, Changsha, 410208, China.

出版信息

Neurochem Res. 2024 Aug;49(8):1965-1979. doi: 10.1007/s11064-024-04161-5. Epub 2024 Jun 4.

Abstract

Cerebral ischemia-reperfusion injury (CIRI) is the second leading cause of death worldwide, posing a huge risk to human life and health. Therefore, investigating the pathogenesis underlying CIRI and developing effective treatments are essential. Ferroptosis is an iron-dependent mode of cell death, which is caused by disorders in iron metabolism and lipid peroxidation. Previous studies demonstrated that ferroptosis is also a form of autophagic cell death, and nuclear receptor coactivator 4(NCOA4) mediated ferritinophagy was found to regulate ferroptosis by interfering with iron metabolism. Ferritinophagy and ferroptosis are important pathogenic mechanisms in CIRI. This review mainly summarizes the link and regulation between ferritinophagy and ferroptosis and further discusses their mechanisms in CIRI. In addition, the potential treatment methods targeting ferritinophagy and ferroptosis for CIRI are presented, providing new ideas for the prevention and treatment of clinical CIRI in the future.

摘要

脑缺血再灌注损伤(CIRI)是全球范围内导致死亡的第二大原因,对人类的生命和健康构成了巨大威胁。因此,研究 CIRI 的发病机制并开发有效的治疗方法至关重要。铁死亡是一种铁依赖性的细胞死亡方式,由铁代谢和脂质过氧化紊乱引起。先前的研究表明,铁死亡也是一种自噬性细胞死亡形式,核受体共激活因子 4(NCOA4)介导的铁蛋白自噬被发现通过干扰铁代谢来调节铁死亡。铁蛋白自噬和铁死亡是 CIRI 的重要发病机制。本综述主要总结了铁蛋白自噬和铁死亡之间的联系和调节,并进一步探讨了它们在 CIRI 中的机制。此外,还提出了针对 CIRI 中铁蛋白自噬和铁死亡的潜在治疗方法,为未来临床 CIRI 的防治提供了新的思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce3b/11233298/224058a76b8b/11064_2024_4161_Fig1_HTML.jpg

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