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自噬与铁死亡之间的相互作用及其在缺血性卒中中的潜在作用

Crosstalk Between Autophagy and Ferroptosis and Its Putative Role in Ischemic Stroke.

作者信息

Liu Jie, Guo Zhen-Ni, Yan Xiu-Li, Huang Shuo, Ren Jia-Xin, Luo Yun, Yang Yi

机构信息

Department of Neurology, Stroke Center & Clinical Trial and Research Center for Stroke, The First Hospital of Jilin University, Changchun, China.

China National Comprehensive Stroke Center, Changchun, China.

出版信息

Front Cell Neurosci. 2020 Oct 2;14:577403. doi: 10.3389/fncel.2020.577403. eCollection 2020.

DOI:10.3389/fncel.2020.577403
PMID:33132849
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7566169/
Abstract

Autophagy is a conserved process to maintains homeostasis via the degradation of toxic cell contents, which can either promote cell survival or accelerate cellular demise. Ferroptosis is a recently discovered iron-dependent cell death pathway associated with the accumulation of lethal reactive lipid species. In the past few years, an increasing number of studies have suggested the crosstalk between autophagy and ferroptosis. Ischemic stroke is a complex brain disease regulated by several cell death pathways, including autophagy and ferroptosis. However, the potential links between autophagy and ferroptosis in ischemic stroke have not yet been explored. In this review, we briefly overview the mechanisms of ferroptosis and autophagy, as well as their possible connections in ischemic stroke. The elucidation of crosstalk between different cell death pathways may provide insight into new future ischemic stroke therapies.

摘要

自噬是一种通过降解有毒细胞成分来维持体内平衡的保守过程,这一过程既可以促进细胞存活,也可以加速细胞死亡。铁死亡是最近发现的一种与致死性反应性脂质物质积累相关的铁依赖性细胞死亡途径。在过去几年中,越来越多的研究表明自噬与铁死亡之间存在相互作用。缺血性中风是一种受多种细胞死亡途径(包括自噬和铁死亡)调节的复杂脑部疾病。然而,缺血性中风中自噬与铁死亡之间的潜在联系尚未得到探索。在这篇综述中,我们简要概述了铁死亡和自噬的机制,以及它们在缺血性中风中可能的联系。阐明不同细胞死亡途径之间的相互作用可能为未来缺血性中风的新疗法提供思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f495/7566169/cf2186dc11b3/fncel-14-577403-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f495/7566169/ae2f39e12065/fncel-14-577403-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f495/7566169/cf2186dc11b3/fncel-14-577403-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f495/7566169/ae2f39e12065/fncel-14-577403-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f495/7566169/cf2186dc11b3/fncel-14-577403-g002.jpg

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