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局部和全身给予胰高血糖素样肽-1受体(GLP-1R)激动剂均可挽救高血压性青光眼患者的视网膜神经节细胞。

Topical and systemic GLP-1R agonist administration both rescue retinal ganglion cells in hypertensive glaucoma.

作者信息

Lawrence Emily C N, Guo Michelle, Schwartz Turner D, Wu Jie, Lu Jingwen, Nikonov Sergei, Sterling Jacob K, Cui Qi N

机构信息

Department of Ophthalmology, Scheie Eye Institute, University of Pennsylvania, Philadelphia, PA, United States.

出版信息

Front Cell Neurosci. 2023 Jun 9;17:1156829. doi: 10.3389/fncel.2023.1156829. eCollection 2023.

Abstract

Glaucomatous neurodegeneration, a blinding disease affecting millions worldwide, has a need for the exploration of new and effective therapies. Previously, the glucagon-like peptide-1 receptor (GLP-1R) agonist NLY01 was shown to reduce microglia/macrophage activation, rescuing retinal ganglion cells after IOP elevation in an animal model of glaucoma. GLP-1R agonist use is also associated with a reduced risk for glaucoma in patients with diabetes. In this study, we demonstrate that several commercially available GLP-1R agonists, administered either systemically or topically, hold protective potential in a mouse model of hypertensive glaucoma. Further, the resulting neuroprotection likely occurs through the same pathways previously shown for NLY01. This work contributes to a growing body of evidence suggesting that GLP-1R agonists represent a viable therapeutic option for glaucoma.

摘要

青光眼性神经退行性变是一种影响全球数百万人的致盲疾病,需要探索新的有效治疗方法。此前,在青光眼动物模型中,胰高血糖素样肽-1受体(GLP-1R)激动剂NLY01被证明可减少小胶质细胞/巨噬细胞激活,在眼压升高后挽救视网膜神经节细胞。使用GLP-1R激动剂还与糖尿病患者患青光眼的风险降低有关。在本研究中,我们证明,几种市售的GLP-1R激动剂,无论是全身给药还是局部给药,在高血压性青光眼小鼠模型中都具有保护潜力。此外,由此产生的神经保护作用可能通过先前在NLY01中显示的相同途径发生。这项工作为越来越多的证据做出了贡献,表明GLP-1R激动剂是青光眼的一种可行治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38de/10288152/331110fc9efb/fncel-17-1156829-g001.jpg

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