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青光眼中的神经胶质细胞:朋友、敌人及潜在治疗靶点

Glial Cells in Glaucoma: Friends, Foes, and Potential Therapeutic Targets.

作者信息

García-Bermúdez Mariana Y, Freude Kristine K, Mouhammad Zaynab A, van Wijngaarden Peter, Martin Keith K, Kolko Miriam

机构信息

Department of Drug Design and Pharmacology, University of Copenhagen, Copenhagen, Denmark.

Department for Veterinary and Animal Science, University of Copenhagen, Copenhagen, Denmark.

出版信息

Front Neurol. 2021 Mar 16;12:624983. doi: 10.3389/fneur.2021.624983. eCollection 2021.

DOI:10.3389/fneur.2021.624983
PMID:33796062
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8007906/
Abstract

Glaucoma is the second leading cause of blindness worldwide, affecting ~80 million people by 2020 (1, 2). The condition is characterized by a progressive loss of retinal ganglion cells (RGCs) and their axons accompanied by visual field loss. The underlying pathophysiology of glaucoma remains elusive. Glaucoma is recognized as a multifactorial disease, and lowering intraocular pressure (IOP) is the only treatment that has been shown to slow the progression of the condition. However, a significant number of glaucoma patients continue to go blind despite intraocular pressure-lowering treatment (2). Thus, the need for alternative treatment strategies is indisputable. Accumulating evidence suggests that glial cells play a significant role in supporting RGC function and that glial dysfunction may contribute to optic nerve disease. Here, we review recent advances in understanding the role of glial cells in the pathophysiology of glaucoma. A particular focus is on the dynamic and essential interactions between glial cells and RGCs and potential therapeutic approaches to glaucoma by targeting glial cells.

摘要

青光眼是全球第二大致盲原因,到2020年影响约8000万人(1, 2)。该病的特征是视网膜神经节细胞(RGCs)及其轴突逐渐丧失,并伴有视野缺损。青光眼的潜在病理生理学机制仍不清楚。青光眼被认为是一种多因素疾病,降低眼压(IOP)是唯一已被证明能减缓病情进展的治疗方法。然而,尽管进行了降低眼压的治疗,仍有相当数量的青光眼患者继续失明(2)。因此,需要替代治疗策略是无可争议的。越来越多的证据表明,神经胶质细胞在支持RGC功能方面发挥着重要作用,神经胶质细胞功能障碍可能导致视神经疾病。在这里,我们综述了在理解神经胶质细胞在青光眼病理生理学中的作用方面的最新进展。特别关注神经胶质细胞与RGCs之间动态且重要的相互作用,以及通过靶向神经胶质细胞治疗青光眼的潜在方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d0a/8007906/dd89330fbd81/fneur-12-624983-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d0a/8007906/86308d182f17/fneur-12-624983-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d0a/8007906/ca199bafb143/fneur-12-624983-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d0a/8007906/dd89330fbd81/fneur-12-624983-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d0a/8007906/86308d182f17/fneur-12-624983-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d0a/8007906/ca199bafb143/fneur-12-624983-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d0a/8007906/dd89330fbd81/fneur-12-624983-g0003.jpg

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Interleukin-10 Prevents Pathological Microglia Hyperactivation following Peripheral Endotoxin Challenge.
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bioRxiv. 2025 Jun 25:2025.06.20.660800. doi: 10.1101/2025.06.20.660800.
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Preclinical Retinal Disease Models: Applications in Drug Development and Translational Research.临床前视网膜疾病模型:在药物开发和转化研究中的应用
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