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GLP-1 Receptor Agonist NLY01 Reduces Retinal Inflammation and Neuron Death Secondary to Ocular Hypertension.GLP-1 受体激动剂 NLY01 可降低眼高压继发的视网膜炎症和神经元死亡。
Cell Rep. 2020 Nov 3;33(5):108271. doi: 10.1016/j.celrep.2020.108271.
2
Early life overnutrition impairs plasticity of non-neuronal brainstem cells and drives obesity in offspring across development in rats.早期生活营养过剩会损害非神经元脑干细胞的可塑性,并在大鼠的整个发育过程中导致后代肥胖。
Int J Obes (Lond). 2020 Dec;44(12):2405-2418. doi: 10.1038/s41366-020-00658-5. Epub 2020 Sep 30.
3
Neurotoxic Reactive Astrocytes Drive Neuronal Death after Retinal Injury.神经毒性反应性星形胶质细胞在视网膜损伤后导致神经元死亡。
Cell Rep. 2020 Jun 23;31(12):107776. doi: 10.1016/j.celrep.2020.107776.
4
Semaglutide lowers body weight in rodents via distributed neural pathways.司美格鲁肽通过分布式神经通路降低啮齿动物的体重。
JCI Insight. 2020 Mar 26;5(6):133429. doi: 10.1172/jci.insight.133429.
5
Liraglutide Up-regulation Thioredoxin Attenuated Müller Cells Apoptosis in High Glucose by Regulating Oxidative Stress and Endoplasmic Reticulum Stress.利拉鲁肽上调硫氧还蛋白减轻高糖诱导的 Muller 细胞凋亡及其机制研究。
Curr Eye Res. 2020 Oct;45(10):1283-1291. doi: 10.1080/02713683.2020.1737137. Epub 2020 Mar 17.
6
Dorsal vagal complex and hypothalamic glia differentially respond to leptin and energy balance dysregulation.背侧迷走复合体和下丘脑神经胶质对瘦素和能量平衡失调的反应不同。
Transl Psychiatry. 2020 Mar 9;10(1):90. doi: 10.1038/s41398-020-0767-0.
7
GABA neurons in the nucleus tractus solitarius express GLP-1 receptors and mediate anorectic effects of liraglutide in rats.孤束核中的 GABA 神经元表达 GLP-1 受体,并介导利拉鲁肽对大鼠的摄食抑制作用。
Sci Transl Med. 2020 Mar 4;12(533). doi: 10.1126/scitranslmed.aay8071.
8
Improved tools to study astrocytes.改进的星形胶质细胞研究工具。
Nat Rev Neurosci. 2020 Mar;21(3):121-138. doi: 10.1038/s41583-020-0264-8. Epub 2020 Feb 10.
9
Regulation of food intake by astrocytes in the brainstem dorsal vagal complex.脑桥背侧迷走复合体星形胶质细胞对摄食的调节作用。
Glia. 2020 Jun;68(6):1241-1254. doi: 10.1002/glia.23774. Epub 2019 Dec 27.
10
THE CONCISE GUIDE TO PHARMACOLOGY 2019/20: Introduction and Other Protein Targets.2019/20 年简明药理学指南:引言和其他蛋白靶点。
Br J Pharmacol. 2019 Dec;176 Suppl 1(Suppl 1):S1-S20. doi: 10.1111/bph.14747.

胶质细胞在胰高血糖素样肽-1 的生理学和药理学中的作用:对肥胖、糖尿病、神经退行性变和青光眼的影响。

The role of glia in the physiology and pharmacology of glucagon-like peptide-1: implications for obesity, diabetes, neurodegeneration and glaucoma.

机构信息

Scheie Eye Institute, Philadelphia, Pennsylvania, USA.

Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.

出版信息

Br J Pharmacol. 2022 Feb;179(4):715-726. doi: 10.1111/bph.15683. Epub 2021 Nov 23.

DOI:10.1111/bph.15683
PMID:34519040
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8820182/
Abstract

The medical applications of glucagon-like peptide-1 receptor (GLP-1R) agonists is evergrowing in scope, highlighting the urgent need for a comprehensive understanding of the mechanisms through which GLP-1R activation impacts physiology and behaviour. A new area of research aims to elucidate the role GLP-1R signalling in glia, which play a role in regulating energy balance, glycemic control, neuroinflammation and oxidative stress. Once controversial, existing evidence now suggests that subsets of glia (e.g. microglia, tanycytes and astrocytes) and infiltrating macrophages express GLP-1Rs. In this review, we discuss the implications of these findings, with particular focus on the effectiveness of both clinically available and novel GLP-1R agonists for treating metabolic and neurodegenerative diseases, enhancing cognition and combating substance abuse. LINKED ARTICLES: This article is part of a themed issue on GLP1 receptor ligands (BJP 75th Anniversary). To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v179.4/issuetoc.

摘要

胰高血糖素样肽-1 受体 (GLP-1R) 激动剂在医学上的应用范围不断扩大,这突显了人们迫切需要全面了解 GLP-1R 激活对生理和行为的影响机制。一个新的研究领域旨在阐明 GLP-1R 信号在神经胶质中的作用,神经胶质在调节能量平衡、血糖控制、神经炎症和氧化应激方面发挥作用。虽然曾经存在争议,但现有证据表明,神经胶质的某些亚群(如小神经胶质细胞、室管膜细胞和星形胶质细胞)和浸润的巨噬细胞表达 GLP-1R。在这篇综述中,我们讨论了这些发现的意义,特别关注临床可用和新型 GLP-1R 激动剂在治疗代谢和神经退行性疾病、增强认知和对抗物质滥用方面的有效性。相关文章:本文是 GLP1 受体配体专题(BJP 75 周年纪念)的一部分。要查看本节中的其他文章,请访问 http://onlinelibrary.wiley.com/doi/10.1111/bph.v179.4/issuetoc.