ArticleThe Kaohsiung journal of medical sciences2023
Suppression of cAMP/PKA/CREB signaling ameliorates retinal injury in diabetic retinopathy.
Article in The Kaohsiung journal of medical sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Retinal VIP-amacrine cells: their development, structure, and function.Eye (London, England) · 2024Pooled it
- cAMP-response element binding protein (CREB)-mediated glycolysis enhancement promotes apoptosis of RAW264.7 macrophages infected with BCG under high glucose conditions.BMC microbiology · 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
- Scutellarin attenuates high glucose-induced edema and inflammation in retinal Müller cells via AQP4/Kir4.1 restoration and TLR4/MyD88/NF-κB inhibition.Frontiers in pharmacology · 2026Article
- Zinc-Related Proteasome Variants in Type 1 Diabetes: An in Silico-Guided Case-Control Study.Metabolites · 2025Article
- Bipolar and schizophrenia risk gene AKAP11 encodes an autophagy receptor coupling the regulation of PKA kinase network homeostasis to synaptic transmission.Nature communications · 2025Article
- From disruption to remodeling: the evolution and therapeutic prospects of Neuroimmune Regulatory Circuitry after ischemic stroke.Frontiers in immunology · 2025Review
- Fenofibrate mitigates the dysfunction of high glucose-driven human retinal microvascular endothelial cells by suppressing NLRP3 inflammasome.International journal of ophthalmology · 2025Article
- Hhatl Reduces Apoptosis of Müller Cells in Diabetic Retinopathy by Relieving Endoplasmic Reticulum Stress.International journal of endocrinology · 2025Article
- Emodin inhibits benzidine‑enhanced survival and migration of upper urinary tract urothelial carcinoma cells by targeting the PKA/COX2 signaling pathway.International journal of oncology · 2024Article
- From Nature to Treatment: The Impact of Pterostilbene on Mitigating Retinal Ischemia-Reperfusion Damage by Reducing Oxidative Stress, Inflammation, and Apoptosis.Life (Basel, Switzerland) · 2024Article
- Exploring early DNA methylation alterations in type 1 diabetes: implications of glycemic control.Frontiers in endocrinology · 2024Article
- Suppression of cAMP/PKA/CREB signaling ameliorates retinal injury in diabetic retinopathy.The Kaohsiung journal of medical sciences · 2023Article
- Yigan Mingmu Decoction inhibits diabetic macular edema through regulating Kir4.1/AQP4 axis: a study based on network pharmacology.American journal of translational research · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The blood-retinal barrier (BRB), homeostasis, neuronal integrity, and metabolic processes are all directly influenced by Müller cells, the most important retinal glial cells. We isolated primary Müller cells from Sprague-Dawley (SD) neonatal rats and treated them with glucose at varying doses. CCK-8 was used to quantify cellular viability, and a TUNEL assay was performed to detect cell apoptosis. ELISA, immunofluorescence, and western blotting were used to assess cAMP/PKA/CREB signaling, Kir4.1, AQP4, GFAP, and VEGF levels, respectively. H&E staining was used to examine histopathological alterations in diabetic retinopathy (DR)-affected retinal tissue in rats. As glucose concentration increases, gliosis of Müller cells became apparent, as evidenced by a decline in cell activity, an increase in apoptosis, downregulation of Kir4.1 level, and overexpression of GFAP, AQP4, and VEGF. Treatments with low, intermediate, and high glucose levels led to aberrant activation of cAMP/PKA/CREB signaling. Interestingly, blocking cAMP and PKA reduced high glucose-induced Müller cell damage and gliosis by a significant amount. Further in vivo results suggested that cAMP or PKA inhibition significantly improved edema, bleeding, and retinal disorders. Our findings showed that high glucose exacerbated Müller cell damage and gliosis via a mechanism involving cAMP/PKA/CREB signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.