ArticleProstaglandins & other lipid mediators2024
12-HETE activates Müller glial cells: The potential role of GPR31 and miR-29.
Article in Prostaglandins & other lipid mediators, 2024. 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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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Article
- [Establishment and application of a knowledge-directed pseudo-targeted analytical method for diabetic retinopathy].Se pu = Chinese journal of chromatography · 2026Article
- Lipoxin B4 Mitigates TRPV4-Activated Müller Cell Gliosis During Ocular Hypertension.Investigative ophthalmology & visual science · 2026Article
- Systemic strategies to prevent early diabetic retinopathy: targeting polyunsaturated fatty acid metabolism and eicosanoid signaling.Frontiers in medicine · 2026Review
- Alterations of Bioactive Lipid Profiles in the Retina Following Traumatic Optic Neuropathy in Mice.Biomolecules · 2025Article
- Lipoxin BbioRxiv : the preprint server for biology · 2025Article
- Mir-509-3p targets SLC25A13 to regulate ferroptosis and protect retinal endothelial cells in diabetic retinopathy.Acta diabetologica · 2025Article
- Article
- The Role of microRNAs Related to Apoptosis forInternational journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Diabetic retinopathy (DR) is a neurovascular complication of diabetes, driven by an intricate network of cellular and molecular mechanisms. This study sought to explore the mechanisms by investigating the role of 12-hydroxyeicosatetraenoic acid (12-HETE), its receptor GPR31, and microRNA (miR-29) in the context of DR, specifically focusing on their impact on Müller glial cells. We found that 12-HETE activates Müller cells (MCs), elevates glutamate production, and induces inflammatory and oxidative responses, all of which are instrumental in DR progression. The expression of GPR31, the receptor for 12-HETE, was prominently found in the retina, especially in MCs and retinal ganglion cells, and was upregulated in diabetes. Interestingly, miR29 showed potential as a protective agent, mitigating the harmful effects of 12-HETE by attenuating inflammation and oxidative stress, and restoring the expression of pigment epithelium-derived factor (PEDF). Our results underline the central role of 12-HETE in DR progression through activation of a neurovascular toxic pathway in MCs and illuminate the protective capabilities of miR-29, highlighting both as promising therapeutic targets for the management of DR.
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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.