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
过氧化物,谷氨酸
【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
【中图分类号】 R 722.1 【文献标识码】 A DOI:10.12114/j.issn.1007-9572.2024.0254
Research Progress on the Mechanism of Ferroptosis in Neonatal Hypoxic-ischemic Brain Damage
【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 ......
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