ArticleFunctional & integrative genomics2025
Epigenetic silencing of MSTN via m6A modification underlies the renoprotective effects of engineered MSC exosomes with RBM15 depletion in diabetic nephropathy.
Article in Functional & integrative genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- From pathogenic carriers to therapeutic hope: the dual role and translational prospects of exosomes in diabetic kidney disease.Frontiers in endocrinology · 2026Review
- Mesenchymal Stem Cell Therapy for Type 2 Diabetes: Synergistic β-Cell Regeneration, Immune Modulation, and Exosome-Mediated Glucose Homeostasis.Stem cells international · 2026Review
- Harnessing myostatin pleiotropy for multitrait improvement via precision gene editing.Frontiers in genome editing · 2026Review
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Authors and funding
5 authors.
Funding
Abstract
Diabetic nephropathy (DN) is a leading complication of diabetes mellitus. Engineered exosomes have shown promise in disease treatment by enabling targeted cargo delivery. RNA-binding motif protein 15 (RBM15) accelerates the progression of DN. This study developed siRBM15-loaded exosomes and evaluated their therapeutic efficacy and mechanisms. Exosomes were isolated from human umbilical cord MSCs (hucMSCs) and loaded with siRBM15 (siRBM15-Exo) by electroporation. Human glomerular mesangial cells (HGMCs) were exposed to high glucose (HG). A rat model of DN was generated by streptozotocin induction. The effects on cell pathological responses were evaluated by detecting α-SMA and collagen IV expression, TNF-α and IL-1β levels, ROS and MDA levels, SOD activity, the percentage of SA-β-gal positive cells, and senescence-associated factors p53 and p21. The impact on DN rats was assessed by measuring pathological changes and inflammation. Myostatin (MSTN) and RBM15 were overexpressed in DN kidneys and HG-stimulated HGMCs. MSTN depletion reduced the production of the related markers of fibrosis, inflammation, oxidative stress, and senescence in HG-stimulated HGMCs. Mechanistically, RBM15 stabilized MSTN mRNA via m6A methylation. Reintroducing MSTN reversed these protective effects of RBM15 silencing on HG-induced pathological responses in HGMCs. Furthermore, siRBM15-Exo attenuated HG-induced fibrotic, inflammatory, oxidative, and senescent responses in HGMCs and mitigated inflammation and pathological changes in DN rats. SiRBM15-Exo downregulated MSTN in HG-stimulated HGMCs. Our study shows that the siRBM15-Exo effectively suppress MSTN expression to alleviate DN progression, providing promising translational potential for DN therapy.
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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.