ArticleJournal of ophthalmology2025
miR-16-5p Regulates Proliferation and Apoptosis in High Glucose-Treated Human Retinal Microvascular Endothelial Cells by Targeting VEGFA and TGFBR1.
Article in Journal of ophthalmology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Emerging mechanisms in dry eye disease: apoptosis-associated tear MicroRNAs and toxicant-related alterations of the glycocalyx and lipid rafts.Frontiers in ophthalmology · 2026Article
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
Diabetic retinopathy (DR) is a common complication of diabetes and the main cause of vision loss in the middle-aged and elderly people. miRNAs play vital roles in the development of DR. This study aimed to explore the effects of miR-16-5p on high glucose (HG)-stimulated human retinal microvascular endothelial cells (HRECs) by modulating vascular endothelial growth factor A (VEGFA) and transforming growth factor beta receptor 1 (TGFBR1). HRECs were treated with 5 mM, 10 mM, 20 mM, and 30 mM of HG to induce the DR cell model. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of miR-16-5p and mRNAs of VEGFA and TGFBR1. Western blot was used to examine VEGFA and TGFBR1 protein levels. The 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide assay was conducted to test cell proliferation. Flow cytometry with Annexin V-FITC/PI double staining was carried out to assess cell apoptosis ratio. Dual-luciferase assay was used to identify the target relationship between miR-16-5p and VEGFA and TGFBR1. Results found that the expression of miR-16-5p in HG-treated HRECs was reduced, and VEGFA and TGFBR1 expressions were upregulated. Knockdown of miR-16-5p increased VEGFA and TGFBR1 mRNA and protein levels, promoted cell proliferation, and inhibited apoptosis in HG-treated HRECs. VEGFA and TGFBR1 inhibition reversed the effect of knocking down miR-16-5p on HRECs. Dual-luciferase reporter assay revealed that VEGFA and TGFBR1 were the target of miR-16-5p. Overall, knockdown of miR-16-5p enhances proliferation and inhibits apoptosis of HRECs by upregulating VEGFA and TGFBR1 expression.
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.