ArticleExperimental & molecular medicine2018
Exendin-4 ameliorates high glucose-induced fibrosis by inhibiting the secretion of miR-192 from injured renal tubular epithelial cells.
Article in Experimental & molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Extracellular vesicles carrying miRNAs in kidney diseases: a systemic review.Clinical and experimental nephrology · 2020Pooled it
- The dual role of exosomes in renal fibrosis and their potential for clinical translational applications.Renal failure · 2026Review
- Histone deacetylase 3‑mediated histone deacetylation combined with activating transcription factor 3 promotes renal fibrosis by inhibiting Klotho.Molecular medicine reports · 2026Article
- Inflammation, Apoptosis, and Fibrosis in Diabetic Nephropathy: Molecular Crosstalk in Proximal Tubular Epithelial Cells and Therapeutic Implications.Current issues in molecular biology · 2025Review
- MiR-192-5p targets cell cycle regulation in diabetic kidney disease via cyclin-dependent kinase inhibitor 3.Non-coding RNA research · 2025Article
- Managing cardiovascular events, hyperglycemia, and obesity in type 2 diabetes through microRNA regulation linked to glucagon-like peptide-1 receptor agonists.Diabetology & metabolic syndrome · 2025Review
- G protein-coupled receptor-mediated renal fibrosis: a key focus on kidney disease drug development.Frontiers in pharmacology · 2025Review
- Liraglutide ameliorates inflammation and fibrosis by downregulating the TLR4/MyD88/NF-κB pathway in diabetic kidney disease.American journal of physiology. Regulatory, integrative and comparative physiology · 2024Article
- Variants inHeliyon · 2024Article
- Transforming Diabetes Care: The Molecular Pathways through Which GLP1-RAs Impact the Kidneys in Diabetic Kidney Disease.Biomedicines · 2024Review
- Extracellular vesicles: emerging roles, biomarkers and therapeutic strategies in fibrotic diseases.Journal of nanobiotechnology · 2023Review
- Kidney fibrosis: from mechanisms to therapeutic medicines.Signal transduction and targeted therapy · 2023Review
- Review
- Roles of microRNA-192 in diabetic nephropathy: the clinical applications and mechanisms of action.Frontiers in endocrinology · 2023Review
- Crocin attenuates endoplasmic reticulum stress in methylglyoxal-induced diabetic nephropathy in male mice: MicroRNAs alterations and glyoxalase 1-Nrf2 signaling pathways.Iranian journal of basic medical sciences · 2022Article
- Novel Insights into the Roles and Mechanisms of GLP-1 Receptor Agonists against Aging-Related Diseases.Aging and disease · 2022Review
- Exendin-4 as a Versatile Therapeutic Agent for the Amelioration of Diabetic Changes.Advanced pharmaceutical bulletin · 2022Review
- Mitochondrial Pathophysiology on Chronic Kidney Disease.International journal of molecular sciences · 2022Review
- Glucagon-Like Peptide 1 Receptor Agonist Improves Renal Tubular Damage in Mice with Diabetic Kidney Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Article
- Inflammation and Oxidative Stress in Diabetic Kidney Disease: The Targets for SGLT2 Inhibitors and GLP-1 Receptor Agonists.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extracellular vesicles (EVs), which contain microRNA (miRNA), constitute a novel means of cell communication that may contribute to the inevitable expansion of renal fibrosis during diabetic kidney disease (DKD). Exendin-4 is effective for treating DKD through its action on GLP1R. However, the effect of exendin-4 on EV miRNA expression and renal cell communication during the development of DKD remains unknown. In this study, we found that EVs derived from HK-2 cells pre-treated with exendin-4 and high glucose (Ex-HG), which were taken up by normal HK-2 cells, resulted in decreased levels of FN and Col-I compared with EVs from HK-2 cells pre-treated with HG alone. Furthermore, we found that pretreatment with HG and exendin-4 may have contributed to a decrease in miR-192 in both HK-2 cells and EVs in a p53-dependent manner. Finally, we demonstrated that the amelioration of renal fibrosis by exendin-4 occurred through a miR-192-GLP1R pathway, indicating a new pathway by which exendin-4 regulates GLP1R. The results of this study suggest that exendin-4 inhibits the transfer of EV miR-192 from HG-induced renal tubular epithelial cells to normal cells, thus inhibiting GLP1R downregulation and protecting renal cells. This study reports a new mechanism by which exendin-4 exerts a protective effect against DKD.
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