ArticleDiabetology & metabolic syndrome2026
miR-103a-3p contributes to diabetic retinopathy progression via suppressing MFN2.
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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiabetic retinopathy (DR), a complication of diabetes, damages microvascular of retina through various molecular pathways. Emerging evidence points to miRNAs as key players in progression of DR. This study aims to investigate whether miR-103a-3p contributes to pathological processes of DR through MFN2.
methodsSerum samples were collected from type 2 diabetes mellitus patients and divided into NDR, NPDR, and PDR groups based on fundus lesions. miR-103a-3p levels in each group were quantified by qRT-PCR. ARPE-19 cells were cultured under high-glucose (HG). Cell viability and apoptosis rates were evaluated by CCK-8 assay and flow cytometry. Activities of MDA and GSH-Px were detected by specific kits. Luciferase reporter gene confirmed MFN2 as a direct target of miR-103a-3p.
resultsClinical sample detection revealed that miR-103a-3p levels were higher in NPDR and PDR patients compared to control and NDR groups, and it was an independent risk factor for DR. In vitro experiments confirmed that HG treatment greatly increased miR-103a-3p levels, decreased cell viability, accelerated apoptosis, elevated MDA content, and reduced GSH-Px activity, while transfection of miR-103a-3p inhibitor reversed these effects. Using luciferase reporter assay, we identified MFN2 as a direct target of miR-103a-3p. Moreover, rescue experiments demonstrated that silencing MFN2 effectively reversed the cell functions induced by miR-103a-3p inhibitor.
conclusionmiR-103a-3p is upregulated in DR and accelerates its progression by directly targeting and inhibiting MFN2 expression. This study suggested the molecular mechanism of miR-103a-3p/MFN2 axis in DR, identifying a novel potential target for early diagnosis and therapy of DR.
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.