ArticleDiabetology & metabolic syndrome2026
miR-501-5p mediates the progression of type 2 diabetic retinopathy by targeting NR2F2.
Article in Diabetology & metabolic syndrome, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiabetic retinopathy (DR), a leading blinding microvascular complication of type 2 diabetes mellitus (T2DM), is projected to affect 161 million people globally by 2045.
methodsThis study enrolled 261 participants (127 T2DM controls and 134 T2DM with DR). Serum miR-501-5p levels were analyzed by qRT-PCR. Human Retinal Microvascular Endothelial Cells (HRMECs) under high-glucose conditions were transfected to modulate miR-501-5p expression or overexpress NR2F2. The miR-501-5p–NR2F2 interaction was verified by dual-luciferase assay. Cell proliferation, VEGF, ROS, and endoplasmic reticulum stress markers (GRP78, CHOP) were assessed.
resultsmiR-501-5p was identified as an independent protective factor for DR, showing significant downregulation in T2DM patients and high diagnostic accuracy (AUC = 0.907). In high-glucose conditions, miR-501-5p overexpression reduced VEGF, ROS, and ER stress markers and improved cell proliferation. NR2F2 was confirmed as a direct target of miR-501-5p, and its overexpression reversed the protective effects of miR-501-5p.
conclusionThese findings suggest that miR-501-5p is strongly associated with DR and may serve as a potential biomarker and protective agent, possibly through targeting NR2F2 to ameliorate high glucose-induced retinal microvascular damage.
Indexed as
Identifiers
What OpenQuestion holds
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.