Chinese General Practice ›› 2025, Vol. 28 ›› Issue (06): 666-672.DOI: 10.12114/j.issn.1007-9572.2024.0254

• Frontiers of Medicine • Previous Articles     Next Articles

Research Progress on the Mechanism of Ferroptosis in Neonatal Hypoxic-ischemic Brain Damage

  

  1. 1. School of Clinical Medicine, Shandong Second Medical University, Weifang 261000, China
    2. Graduate School, Shandong First Medical University, Jinan 250014, China
    3. Department of Pediatrics, Jinan Central Hospital, Jinan 250014, China
  • Received:2024-07-10 Revised:2024-08-28 Published:2025-02-20 Online:2024-11-25
  • Contact: XING Xuexue, BI Meirong

铁死亡在新生儿缺氧缺血性脑损伤中的作用机制研究进展

  

  1. 1.261000 山东省潍坊市,山东第二医科大学临床医学院
    2.250014 山东省济南市,山东第一医科大学研究生部
    3.250014 山东省济南市中心医院儿科
  • 通讯作者: 邢雪雪, 毕玫荣
  • 作者简介:

    作者贡献:

    张天阳提出研究选题方向、构思设计并撰写论文;徐文秀、秦昕宇负责制订检索策略、收集与整理文献;邢雪雪、毕玫荣负责论文的修订、质量控制及审校,并对文章整体负责;所有作者确认了论文的最终稿。

  • 基金资助:
    国家卫生健康委医药卫生科技发展课题(WA2020HK61); 山东省妇幼保健协会2021年度科技创新项目

Abstract:

Neonatal hypoxic-ischemic brain damage (HIBD) is one of the common causes of neurological injuries in the neonatal period, which is prone to lead to high disability and mortality in newborns, and its pathogenesis is complex and there is no specific treatment in the clinic. Ferroptosis, as a newly discovered type of non-apoptotic cell death in recent years, has received widespread attention and has gradually become a research hotspot. Research on ferroptosis and neonatal HIBD has been increasing year by year, and a large number of studies have shown that ferroptosis is closely related to the occurrence and development of neonatal HIBD. Moreover, it has been pointed out that vitamin K2, especially MK-4, can exert its neuroprotective effect by inhibiting ferroptosis. In this paper, we briefly review the mechanism of ferroptosis in neonatal HIBD and microglia, and look forward to the possibility that vitamin K2, especially MK-4, can improve the prognosis of neonatal HIBD by inhibiting ferroptosis, with the aim of providing a more economical, safer, and more targeted treatment.

Key words: Brain injuries, Ferroptosis, Neonatal hypoxic-ischemic brain damage, Lipid peroxidation, MK-4, Microglia, Review

摘要:

新生儿缺氧缺血性脑损伤(HIBD)是新生儿期神经系统损伤的常见原因之一,易导致新生儿高致残率、高死亡率,其发病机制复杂且在临床上无特异性治疗方法。铁死亡作为近年新发现的一种非凋亡性细胞死亡类型,受到广泛关注并逐渐成为研究热点。关于铁死亡与新生儿HIBD的研究逐年增多,大量研究表明铁死亡与新生儿HIBD的发生、发展密切相关。并且,有研究指出维生素K2,特别是甲萘醌-4(MK-4)可以通过抑制铁死亡发挥其神经保护作用。本文简要综述铁死亡在新生儿HIBD及小胶质细胞中的作用机制,并展望维生素K2,特别是MK-4通过抑制铁死亡改善新生儿HIBD预后的可能,以期提供一种更加经济、安全且更具针对性的治疗方式。

关键词: 脑损伤, 铁死亡, 新生儿缺氧缺血性脑损伤, 脂质过氧化作用, 甲萘醌-4, 小胶质细胞, 综述

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