ArticleJournal of advanced research2026
Epac1 deletion attenuates Müller glial pathological activation and mitigates retinal neurodegeneration in ischemia-induced retinopathy.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- ScRNA-seq Data Reveal Gene Upregulation and Downregulation in Oxygen-Induced Retinopathy.Medical science monitor : international medical journal of experimental and clinical research · 2026Article
- The impact of anti-vascular endothelial growth factor therapy on the activation status of retinal macrophages/microglia in patients with diabetic retinopathy and familial exudative vitreoretinopathy and its association with treatment response.American journal of translational research · 2026Article
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Authors and funding
9 authors.
Funding
Abstract
introductionIschemia-induced retinopathies, such as retinopathy of prematurity and proliferative diabetic retinopathy, are major causes of vision loss. Both pathological neovascularization and neuronal damage contribute to vision impairment in these conditions, yet current therapies primarily target neovascularization and may further compromise neuronal health.
objectivesCyclic AMP (cAMP) is a widely recognized second messenger regulating diverse physiological and pathological processes. Exchange protein directly activated by cAMP (Epac) is a recently identified effector of cAMP signaling. This study aimed to investigate the role of Epac1 in ischemia-induced retinopathy and elucidate its underlying mechanisms using a mouse model of oxygen-induced retinopathy (OIR).
methodsA mouse OIR model was established by exposing pups to 70% oxygen from postnatal day 7 (P7) to P12. Retinal structure and neuronal survival were assessed by H&E staining, TUNEL assay and immunostaining. Single-cell RNA sequencing (scRNA-seq), immunostaining, qPCR, Western blot, and proximity ligation assay were used to investigate cellular and molecular mechanisms by which Epac1 contributes to retinal pathology in OIR.
resultsGenetic deletion of Epac1 significantly protected against retinal neuronal loss and attenuated Müller glial activation in addition to reducing pathological neovascularization and promoting vascular repair. scRNA-seq revealed substantial transcriptomic alterations in Müller cells during OIR, including the emergence of reactive subclusters with distinct pathological roles, which were mitigated by Epac1 deletion. At the molecular level, Epac1 deletion restored ischemia-reduced VEGFR2 level in Müller cells during OIR, while Epac activation promoted VEGFR2 internalization and impaired VEGF signaling and its neuroprotective effects in primary Müller cells.
conclusionThese findings reveal a novel role for Epac1 in promoting retinal neurodegeneration in a mouse model of OIR through modulation of VEGF signaling in Müller cells. Targeting Epac1 may thus provide therapeutic benefit by preserving neuronal integrity in addition to its effects on vascular pathology.
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