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本文引用的文献

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HMGB1 coordinates SASP-related chromatin folding and RNA homeostasis on the path to senescence.HMGB1 协调 SASP 相关染色质折叠和 RNA 动态平衡,从而走向衰老。
Mol Syst Biol. 2021 Jun;17(6):e9760. doi: 10.15252/msb.20209760.
2
CD4 T cells mediate brain inflammation and neurodegeneration in a mouse model of Parkinson's disease.CD4 T 细胞在帕金森病小鼠模型中介导脑部炎症和神经退行性变。
Brain. 2021 Aug 17;144(7):2047-2059. doi: 10.1093/brain/awab103.
3
Endothelial HMGB1 Is a Critical Regulator of LDL Transcytosis via an SREBP2-SR-BI Axis.内皮细胞高迁移率族蛋白 B1 通过 SREBP2-SR-BI 轴调控 LDL 跨细胞转运。
Arterioscler Thromb Vasc Biol. 2021 Jan;41(1):200-216. doi: 10.1161/ATVBAHA.120.314557. Epub 2020 Oct 15.
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Regulation of Neurogenesis in Mouse Brain by HMGB1.HMGB1 对小鼠大脑神经发生的调控。
Cells. 2020 Jul 17;9(7):1714. doi: 10.3390/cells9071714.
5
HMGB1 A box protects neurons by potently inhibiting both microglia and T cell-mediated inflammation in a mouse Parkinson's disease model.高迁移率族蛋白 B1 通过强烈抑制小胶质细胞和 T 细胞介导的炎症来保护神经元,在小鼠帕金森病模型中。
Clin Sci (Lond). 2020 Aug 14;134(15):2075-2090. doi: 10.1042/CS20200553.
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Reversing a model of Parkinson's disease with in situ converted nigral neurons.利用原位转化的黑质神经元逆转帕金森病模型。
Nature. 2020 Jun;582(7813):550-556. doi: 10.1038/s41586-020-2388-4. Epub 2020 Jun 24.
7
Diagnosis and Treatment of Parkinson Disease: A Review.帕金森病的诊断与治疗:综述。
JAMA. 2020 Feb 11;323(6):548-560. doi: 10.1001/jama.2019.22360.
8
Microglial autophagy defect causes parkinson disease-like symptoms by accelerating inflammasome activation in mice.小胶质细胞自噬缺陷通过加速小鼠炎性小体激活导致帕金森病样症状。
Autophagy. 2020 Dec;16(12):2193-2205. doi: 10.1080/15548627.2020.1719723. Epub 2020 Jan 31.
9
CXCL12 is involved in α-synuclein-triggered neuroinflammation of Parkinson's disease.CXCL12 参与了帕金森病中 α-突触核蛋白触发的神经炎症。
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10
HMGB1/TLR4 promotes apoptosis and reduces autophagy of hippocampal neurons in diabetes combined with OSA.高迁移率族蛋白 B1/Toll 样受体 4 促进糖尿病合并阻塞性睡眠呼吸暂停中海马神经元的凋亡和自噬减少。
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高迁移率族蛋白B1是帕金森病一个具有潜力且具挑战性的治疗靶点。

HMGB1 is a Potential and Challenging Therapeutic Target for Parkinson's Disease.

作者信息

Tian Yu, Chen Rong, Su Zhaoliang

机构信息

International Genome Center, Jiangsu University, 301 Xuefu Road, Zhenjiang, 212013, Jiangsu, China.

Department of Immunology, School of Medicine, Jiangsu University, Zhenjiang, 212013, China.

出版信息

Cell Mol Neurobiol. 2023 Jan;43(1):47-58. doi: 10.1007/s10571-021-01170-8. Epub 2021 Nov 19.

DOI:10.1007/s10571-021-01170-8
PMID:34797463
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11415213/
Abstract

Parkinson's disease (PD) is one of the most common degenerative diseases of the human nervous system and has a wide range of serious impacts on human health and quality of life. Recently, research targeting high mobility group box 1 (HMGB1) in PD has emerged, and a variety of laboratory methods for inhibiting HMGB1 have achieved good results to a certain extent. However, given that HMGB1 undergoes a variety of intracellular modifications and three different forms of extracellular redox, the possible roles of these forms in PD are likely to be different. General inhibition of all forms of HMGB1 is obviously not ideal and has become one of the biggest obstacles in the clinical application of targeting HMGB1. In this review, pure mechanistic research of HMGB1 and in vivo research targeting HMGB1 were combined, the effects of HMGB1 on neurons and immune cell responses in PD are discussed in detail, and the problems that need to be focused on in the future are addressed.

摘要

帕金森病(PD)是人类神经系统最常见的退行性疾病之一,对人类健康和生活质量有着广泛而严重的影响。近年来,针对帕金森病中高迁移率族蛋白B1(HMGB1)的研究不断涌现,多种抑制HMGB1的实验室方法在一定程度上取得了良好效果。然而,鉴于HMGB1在细胞内会发生多种修饰,在细胞外存在三种不同形式的氧化还原状态,这些形式在帕金森病中可能发挥不同的作用。对所有形式的HMGB1进行一般性抑制显然并不理想,这已成为靶向HMGB1临床应用的最大障碍之一。在本综述中,将HMGB1的纯机制研究与靶向HMGB1的体内研究相结合,详细讨论了HMGB1对帕金森病中神经元和免疫细胞反应的影响,并探讨了未来需要关注的问题。