铁死亡在新生儿缺氧缺血性脑损伤中的作用研究进展
[Research advances in the role of ferroptosis in neonatal hypoxic-ischemic brain damage].
作者信息
Zhu Kai-Yi, Hei Ming-Yan
机构信息
Neonatal Center, Beijing Children's Hospital, Capital Medical University/National Center for Child Health, Beijing 100045, China.
出版信息
Zhongguo Dang Dai Er Ke Za Zhi. 2021 May;23(5):536-541. doi: 10.7499/j.issn.1008-8830.2102045.
Abstract
Neonatal hypoxic-ischemic brain damage (HIBD) remains an important cause of neonatal death and disability in infants and young children, but it has a complex mechanism and lacks specific treatment methods. As a new type of programmed cell death, ferroptosis has gradually attracted more and more attention as a new therapeutic target. This article reviews the research advances in abnormal iron metabolism, glutamate antiporter dysfunction, and abnormal lipid peroxide regulation which are closely associated with ferroptosis and HIBD.
摘要
新生儿缺氧缺血性脑损伤（HIBD）仍然是婴幼儿死亡和残疾的重要原因，但它机制复杂且缺乏特异性治疗方法。作为一种新型的程序性细胞死亡，铁死亡作为一种新的治疗靶点逐渐受到越来越多的关注。本文综述了与铁死亡和HIBD密切相关的铁代谢异常、谷氨酸反向转运体功能障碍以及脂质过氧化物调节异常的研究进展。
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