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氧化应激与缺血性脑卒中中铁死亡/氧化细胞死亡的串扰:可能的靶点和分子机制。

Crosstalk between Oxidative Stress and Ferroptosis/Oxytosis in Ischemic Stroke: Possible Targets and Molecular Mechanisms.

机构信息

Stroke Center & Clinical Trial and Research Center for Stroke, Department of Neurology, The First Hospital of Jilin University, No. 1 Xinmin Street, Changchun 130021, China.

China National Comprehensive Stroke Center, No. 1 Xinmin Street, Changchun 130021, China.

出版信息

Oxid Med Cell Longev. 2021 May 11;2021:6643382. doi: 10.1155/2021/6643382. eCollection 2021.

DOI:10.1155/2021/6643382
PMID:34055196
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8133868/
Abstract

Oxidative stress is a key cause of ischemic stroke and an initiator of neuronal dysfunction and death, mainly through the overproduction of peroxides and the depletion of antioxidants. Ferroptosis/oxytosis is a unique, oxidative stress-induced cell death pathway characterized by lipid peroxidation and glutathione depletion. Both oxidative stress and ferroptosis/oxytosis have common molecular pathways. This review summarizes the possible targets and the mechanisms underlying the crosstalk between oxidative stress and ferroptosis/oxytosis in ischemic stroke. This knowledge might help to further understand the pathophysiology of ischemic stroke and open new perspectives for the treatment of ischemic stroke.

摘要

氧化应激是缺血性卒中的一个关键病因,也是神经元功能障碍和死亡的启动因素,主要通过过氧化物的过度产生和抗氧化剂的耗竭来实现。铁死亡/细胞凋亡是一种独特的、由氧化应激诱导的细胞死亡途径,其特征是脂质过氧化和谷胱甘肽耗竭。氧化应激和铁死亡/细胞凋亡都有共同的分子途径。本综述总结了缺血性卒中中铁死亡/细胞凋亡与氧化应激相互作用的可能靶点和机制。这些知识可能有助于进一步理解缺血性卒中的病理生理学,并为缺血性卒中的治疗开辟新的视角。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6581/8133868/8b604cf77421/OMCL2021-6643382.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6581/8133868/576beb7b8ebf/OMCL2021-6643382.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6581/8133868/8b604cf77421/OMCL2021-6643382.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6581/8133868/576beb7b8ebf/OMCL2021-6643382.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6581/8133868/8b604cf77421/OMCL2021-6643382.002.jpg

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