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. 2022 Oct 13;12:17152. doi: 10.1038/s41598-022-22140-0

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Ischemia–reperfusion (IR) leads to significant retinal damage. (A) Transient retinal ischemia was induced for 45 min by increasing intraocular pressure (IOP, 120 mm Hg). (B) Ischemic and normotensive retinas collected 6 and 24 h after reperfusion were used for RNA-seq analysis. Retinas collected 7 days after reperfusion were used to study RGC survival. (C) The representative confocal images indicate significant RGC death (Tubb3 as a marker) and reactive gliosis (Gfap and Cd11b as markers) in ischemic retinas 7 days after reperfusion.