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Excitotoxicity-induced endocytosis as a potential target for stroke neuroprotection.

作者信息

Diaz-Guerra Margarita

机构信息

Instituto de Investigaciones Biomédicas "Alberto Sols", Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid (CSIC-UAM), Madrid, Spain.

出版信息

Neural Regen Res. 2021 Feb;16(2):300-301. doi: 10.4103/1673-5374.290892.

DOI:10.4103/1673-5374.290892
PMID:32859784
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7896228/
Abstract
摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db5a/7896228/364d359ac06a/NRR-16-300-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db5a/7896228/364d359ac06a/NRR-16-300-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db5a/7896228/364d359ac06a/NRR-16-300-g001.jpg

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本文引用的文献

1
Excitotoxic targeting of Kidins220 to the Golgi apparatus precedes calpain cleavage of Rap1-activation complexes.兴奋性毒性靶向 Kidins220 到高尔基体，随后钙蛋白酶切割 Rap1 激活复合物。
Cell Death Dis. 2019 Jul 11;10(7):535. doi: 10.1038/s41419-019-1766-z.
2
Prevention of excitotoxicity-induced processing of BDNF receptor TrkB-FL leads to stroke neuroprotection.预防兴奋毒性诱导的脑源性神经营养因子受体 TrkB-FL 加工可导致卒中神经保护。
EMBO Mol Med. 2019 Jul;11(7):e9950. doi: 10.15252/emmm.201809950. Epub 2019 Jun 3.
3
Endocytosis of GluN2B-containing NMDA receptors mediates NMDA-induced excitotoxicity.
间歇性低压缺氧预处理可减轻中风损伤并调节残余神经元的内吞作用。
Front Neurol. 2021 Dec 15;12:750908. doi: 10.3389/fneur.2021.750908. eCollection 2021.
GluN2B 含有 NMDA 受体的内吞作用介导 NMDA 诱导的兴奋性毒性。
Mol Pain. 2017 Jan;13:1744806917701921. doi: 10.1177/1744806917701921.
4
Integral Characterization of Defective BDNF/TrkB Signalling in Neurological and Psychiatric Disorders Leads the Way to New Therapies.神经和精神疾病中BDNF/TrkB信号通路缺陷的综合表征为新疗法指明方向。
Int J Mol Sci. 2017 Jan 28;18(2):268. doi: 10.3390/ijms18020268.
5
Brain ischaemia induces shedding of a BDNF-scavenger ectodomain from TrkB receptors by excitotoxicity activation of metalloproteinases and γ-secretases.脑缺血通过金属蛋白酶和γ-分泌酶的兴奋性毒性激活，诱导TrkB受体上脑源性神经营养因子（BDNF）清除剂胞外域的脱落。
J Pathol. 2016 Apr;238(5):627-40. doi: 10.1002/path.4684. Epub 2016 Feb 24.
6
Imbalance of neurotrophin receptor isoforms TrkB-FL/TrkB-T1 induces neuronal death in excitotoxicity.神经营养因子受体亚型 TrkB-FL/TrkB-T1 的失衡导致兴奋毒性中的神经元死亡。
Cell Death Dis. 2012 Jan 19;3(1):e256. doi: 10.1038/cddis.2011.143.
7
Endocytosis and intracellular trafficking contribute to necrotic neurodegeneration in C. elegans.内吞作用和细胞内运输导致线虫的坏死性神经退行性变。
EMBO J. 2012 Feb 1;31(3):654-66. doi: 10.1038/emboj.2011.447. Epub 2011 Dec 9.
8
Essential role of Hrs in endocytic recycling of full-length TrkB receptor but not its isoform TrkB.T1.Hrs在全长TrkB受体而非其异构体TrkB.T1的内吞再循环中起关键作用。
J Biol Chem. 2009 May 29;284(22):15126-36. doi: 10.1074/jbc.M809763200. Epub 2009 Apr 7.
9
Excitotoxicity-induced endocytosis confers drug targeting in cerebral ischemia.兴奋性毒性诱导的内吞作用赋予脑缺血中的药物靶向性。
Ann Neurol. 2009 Mar;65(3):337-47. doi: 10.1002/ana.21584.
10
Calpain hydrolysis of alpha- and beta2-adaptins decreases clathrin-dependent endocytosis and may promote neurodegeneration.钙蛋白酶对α-和β2-衔接蛋白的水解作用会降低网格蛋白依赖性内吞作用，并可能促进神经退行性变。
J Biol Chem. 2009 May 1;284(18):12447-58. doi: 10.1074/jbc.M804740200. Epub 2009 Feb 24.