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蛛网膜下腔出血后早期脑损伤中的铁死亡:文献综述

Ferroptosis in early brain injury after subarachnoid hemorrhage: review of literature.

作者信息

Kang Junlin, Tian Shilai, Zhang Lei, Yang Gang

机构信息

The First Hospital of Lanzhou University, Lanzhou City, Gansu Province, China.

Gansu Provincial Hospital, Lanzhou City, Gansu Province, China.

出版信息

Chin Neurosurg J. 2024 Feb 13;10(1):6. doi: 10.1186/s41016-024-00357-4.

DOI:10.1186/s41016-024-00357-4
PMID:38347652
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10863120/
Abstract

Spontaneous subarachnoid hemorrhage (SAH), mainly caused by ruptured intracranial aneurysms, is a serious acute cerebrovascular disease. Early brain injury (EBI) is all brain injury occurring within 72 h after SAH, mainly including increased intracranial pressure, decreased cerebral blood flow, disruption of the blood-brain barrier, brain edema, oxidative stress, and neuroinflammation. It activates cell death pathways, leading to neuronal and glial cell death, and is significantly associated with poor prognosis. Ferroptosis is characterized by iron-dependent accumulation of lipid peroxides and is involved in the process of neuron and glial cell death in early brain injury. This paper reviews the research progress of ferroptosis in early brain injury after subarachnoid hemorrhage and provides new ideas for future research.

摘要

自发性蛛网膜下腔出血(SAH)主要由颅内动脉瘤破裂引起,是一种严重的急性脑血管疾病。早期脑损伤(EBI)是指SAH后72小时内发生的所有脑损伤,主要包括颅内压升高、脑血流量减少、血脑屏障破坏、脑水肿、氧化应激和神经炎症。它激活细胞死亡途径,导致神经元和胶质细胞死亡,并与预后不良显著相关。铁死亡的特征是脂质过氧化物的铁依赖性积累,并参与早期脑损伤中神经元和胶质细胞死亡的过程。本文综述了蛛网膜下腔出血后早期脑损伤中铁死亡的研究进展,为未来的研究提供了新思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2ed/10863120/6a96a892f9bb/41016_2024_357_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2ed/10863120/6a96a892f9bb/41016_2024_357_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2ed/10863120/6a96a892f9bb/41016_2024_357_Fig1_HTML.jpg

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本文引用的文献

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Free Radic Biol Med. 2024 Jan;210:416-429. doi: 10.1016/j.freeradbiomed.2023.11.031. Epub 2023 Nov 30.
2
Takinib inhibits microglial M1 polarization and oxidative damage after subarachnoid hemorrhage by targeting TAK1-dependent NLRP3 inflammasome signaling pathway.替卡替尼通过靶向 TAK1 依赖性 NLRP3 炎性小体信号通路抑制蛛网膜下腔出血后小胶质细胞 M1 极化和氧化损伤。
Front Immunol. 2023 Nov 14;14:1266315. doi: 10.3389/fimmu.2023.1266315. eCollection 2023.
3
血红蛋白暴露后人脑动脉中的基因表达变化:对蛛网膜下腔出血中血管反应的影响
Front Physiol. 2025 Apr 3;16:1529113. doi: 10.3389/fphys.2025.1529113. eCollection 2025.
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FASEB J. 2025 Apr 15;39(7):e70488. doi: 10.1096/fj.202403160R.
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Redox Biol. 2025 May;82:103550. doi: 10.1016/j.redox.2025.103550. Epub 2025 Feb 27.
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