ArticleDiabetology & metabolic syndrome2025
Exosomal FOXL1 from bone marrow mesenchymal stem cells activates the METTL3/ATXN2L pathway to ameliorate high glucose-induced human retinal microvascular endothelial cell injury.
Article in Diabetology & metabolic syndrome, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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
5 citing papers in PubMed.
- Milk-derived exosome-based strategy targeting ferroptosis-glycolysis network promotes bone regeneration in diabetic aging comorbidity.Journal of nanobiotechnology · 2026Article
- LIN28A blocks the EndMT process of high glucose-induced HRMECs by stabilizing SIRT6 mRNA.Journal of diabetes investigation · 2026Article
- PTIP inhibits proliferation, migration, and angiogenesis of retinal microvascular endothelial cells in a high-glucose environment.In vitro cellular & developmental biology. Animal · 2026Article
- Genomic Organization, Evolutionary Conservation and Expression ofBiomedicines · 2025Article
- Identification of Novel Biomarkers and Potential Therapeutic Targets for Systemic Sclerosis: An Integrated Analysis of Plasma Proteome-Wide Mendelian Randomization and Transcriptome.Journal of inflammation research · 2025Article
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
backgroundBone marrow mesenchymal stem cells (BMSCs) and their secreted exosomes have been shown to possess therapeutic potential in various diseases, including diabetic retinopathy (DR). Retinal microvascular endothelial cell (RMEC) injury is a key factor in DR, and understanding the underlying molecular mechanisms is crucial for the treatment of DR. The study investigated the role of MSC-derived exosomes in RMEC injury and the underlying mechanism.
methodsHuman retinal microvascular endothelial cells (HRMECs) were exposed to high glucose (HG) to establish an in vitro DR model. Exosomes were isolated from BMSCs using differential centrifugation and co-incubated with HRMECs for functional studies. mRNA expression of ataxin 2 like (ATXN2L), methyltransferase-like 3 (METTL3), and forkhead box L1 (FOXL1) was assessed by quantitative real-time polymerase chain reaction. Protein expression was evaluated by western blotting. Cell viability was measured with a cell counting kit-8 assay, and pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) were analyzed by enzyme-linked immunosorbent assays. Apoptosis was analyzed through flow cytometry. MDA levels, GSH-Px activity, and ROS levels were determined by colorimetric methods and fluorescence microscopy, respectively. The association of METTL3 with ATXN2L and FOXL1 was investigated using a dual-luciferase reporter assay and RNA immunoprecipitation assay.
resultsHG treatment increased the secretion of pro-inflammatory factors, apoptosis rate, and oxidative stress in HRMECs. BMSC-derived exosomes inhibited inflammation, apoptosis and oxidative stress in HRMECs by transferring FOXL1 into HRMECs. FOXL1 functioned as an RNA-binding protein of METTL3, which stabilized ATXN2L mRNA expression through m6A methylation in HRMECs. ATXN2L expression was reduced in DR patients' serum and HG-treated HRMECs. Overexpression of ATXN2L mitigated the high glucose-induced inflammation, apoptosis, and oxidative stress in HRMECs.
conclusionExosomal FOXL1 from BMSCs stabilized METTL3 to increase ATXN2L expression, thus offering a protective effect against high glucose-induced injury in HRMECs. This finding holds clinical significance for the development of targeted therapies for DR.
Indexed as
Identifiers
What Socratic 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 Socratic graph.