ArticleInvestigative ophthalmology & visual science2020
Epac1 Requires AMPK Phosphorylation to Regulate HMGB1 in the Retinal Vasculature.
Article in Investigative ophthalmology & visual science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed, 11 citations in OpenAlex.
- SIRT1 as a potential target for age-related eye diseases: mechanisms and therapeutic strategies.Human cell · 2025Review
- The AMPK/cAMP Metabolic Signaling Axis as a Possible Therapeutic Target for Diabetes.Current molecular medicine · 2025Review
- Role of High Mobility Group Box 1 in Cardiovascular Diseases.Inflammation · 2022Review
- Prohibitin 1 Regulates Inflammatory Mediators and Reactive Oxygen Species in Retinal Endothelial Cells.Journal of clinical medicine · 2022Article
- Emerging Role of cAMP/AMPK Signaling.Cells · 2022Review
- Altered Expressions of Transfer RNA-Derived Small RNAs and microRNAs in the Vitreous Humor of Proliferative Diabetic Retinopathy.Frontiers in endocrinology · 2022Article
- Epac: A Promising Therapeutic Target for Vascular Diseases: A Review.Frontiers in pharmacology · 2022Review
- TNFAIP3 is anti-inflammatory in the retinal vasculature.Molecular vision · 2022Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Purpose: To investigate whether AMP-activated protein kinase (AMPK) is required for the reduction of high mobility group box 1 (HMGB1) by exchange proteins activated by cAMP 1 (Epac1) in the retinal vasculature. Methods: We measured AMPK phosphorylation in normal and diabetic Epac1 floxed and cdh5/Epac1 Cre mice. We also treated primary human retinal endothelial cells (RECs) in normal (5-mM) or high (25-mM) glucose with an Epac1 agonist and AMPK or insulin-like growth factor receptor binding protein 3 siRNA. We measured protein levels of AMPK, sirtuin 1 (SIRT1), and HMGB1. Results: AMPK phosphorylation was reduced in cdh5/Epac1 Cre mice, suggesting that Epac1 regulated AMPK actions. High-glucose culturing conditions reduced AMPK levels in RECs, but the levels were increased by the Epac1 agonist, supporting the idea that Epac1 regulates AMPK. The Epac1 agonist was not able to reduce HMGB1 levels or increase SIRT1 when AMPK was blocked by AMPK siRNA, thus demonstrating that Epac1 requires AMPK to regulate SIRT1 and HMGB1. Conclusions: Epac1 requires AMPK to increase SIRT1 and reduce HMGB1 in the diabetic retinal vasculature. This finding provides another pathway by which Epac1 may protect the retina during diabetes.
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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 Socratic graph.