ArticleIrish journal of medical science2025
AMSC/CXCR4-derived exosomes and miRNA-320 regulate pathological angiogenesis in diabetes.
Article in Irish journal of medical science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- CXCR4: A Promising Novel Strategy for Lung Cancer Treatment.Biomolecules · 2026Review
- Exogenous glucocorticoid dose impacts circulating microRNA expression in patients with adrenal insufficiency due to 21-hydroxylase deficiency.Frontiers in endocrinology · 2026Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
backgroundDiabetic vascular complications present significant clinical challenges, including limited treatment efficacy, high postoperative restenosis rates, and delayed early diagnosis. This study investigates CXCR4-modified adipose-derived mesenchymal stem cells (AMSCs/CXCR4) in regulating pathological endothelial proliferation under hyperglycemic conditions.
aimsThe purpose is to provide new mechanism insights and potential therapeutic targets for early intervention of diabetes-related vascular diseases.
methodsThe CXCR4-overexpressing plasmid was generated via XhoI/EcoRI double digestion, T4 ligation, and column purification, then transfected into AMSCs using Lipofectamine® 3000 to enhance exosome secretion. These exosomes were co-cultured with HG-treated HUVECs. Cell viability and apoptosis were assessed by CCK8 and flow cytometry. AKT/mTOR pathway proteins (total/phosphorylated) were analyzed via Western blot, while qRT-PCR quantified miRNA320, VEGF, and IGF-1 expression.
resultsChronic high glucose stimulated abnormal endothelial cell proliferation (CCK-8/flow cytometry), which was suppressed by AMSCs/CXCR4, reducing proliferation and elevating apoptosis ( 21.723 ± 1.061% apoptosis rate)). High glucose downregulated miRNA320, but AMSCs/CXCR4 restored its expression ( 0.937 ± 0.056 vs. other groups, P < 0.05). Increased miRNA320 correlated with reduced VEGF ((1.101 ± 0.142) and IGF-1 (1.074 ± 0.084) levels, confirming miRNA320-mediated inhibition. Notably, activation of the AKT/mTOR pathway proteins was not affected, indicating that AMSCs/CXCR4 directly inhibited the activity of VEGF and IGF-1 in HUVECs via miRNA320.
conclusionsCXCR4 boosts exosome release from AMSCs. Although AMSCs/CXCR4 did not alter AKT/mTOR signaling, their miRNA320-loaded exosomes blocked IGF-1/VEGF activity. This study uncovers a CXCR4-miRNA320 axis in diabetic vascular dysfunction, highlighting exosome-based therapy and miRNA320 as a targeted strategy for vascular complications.
Indexed as
Identifiers
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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.