ArticleInternational journal of biological sciences2025
Senescent renal tubular cells derived extracellular vesicles transported miR-20a and miR-21 induced macrophage-to-myofibroblast transition in renal fibrosis after ischemia reperfusion injury.
Article in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- The dual role of exosomes in renal fibrosis and their potential for clinical translational applications.Renal failure · 2026Review
- Versatile Microgel Platform for Intervertebral Disc Degeneration Therapy: Targeting Pericyte-Mediated Fibrosis and Protecting Nucleus Pulposus Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Lactate-lactylation circuitry in kidney fibrosis: cellular crosstalk from tubular metabolic reprogramming to macrophage effector functions.Seminars in immunopathology · 2026Review
- Exosomal miR-21-5p from ectopic endometrial stromal cells drives fibrosis progression in endometriosis through direct VHL targeting.Human cell · 2026Article
- MMT: A Potential Mechanism of Myocardial Fibrosis - Regulation of the TGF-β1/Smad3 Pathway and Prospects for Targeted Therapy.Reviews in cardiovascular medicine · 2026Review
- Urinary MicroRNA Expression and Tacrolimus Pharmacokinetic Variability in Kidney Transplant Recipients: A Cross-sectional Study.Clinical drug investigation · 2026Article
- MSC-EVs attenuate subretinal fibrosis in choroidal neovascularization through miR-21-5p-mediated inhibition of EMT and MMT and suppression of inflammation.Journal of neuroinflammation · 2026Article
- Leocarpinolide B alleviates epithelial tubular mitochondrial dysfunction via macrophage exosomal miR-204-5p/TFAM axis in AKI-CKD transition.Journal of nanobiotechnology · 2026Article
- Spatiotemporal Control of Intercellular Crosstalk: A New Therapeutic Paradigm for Halting Acute Kidney Injury to Chronic Kidney Disease Transition.Biomolecules · 2026Review
- MicroRNA Regulation in Kidney Interstitial Fibrosis.Epigenomes · 2026Review
- Cellular senescence of renal tubular epithelial cells in diabetic kidney disease: emerging mechanisms and targeted interventions.Frontiers in cell and developmental biology · 2026Review
- Gut microbial-derived metabolites: key players in kidney disease and renal fibrosis.International journal of biological sciences · 2026Review
- Effects of Chronic Intermittent Hypoxia and Subsequent Normoxic Recovery on Renal Senescence and the PI3K/Akt/P21 Pathway in Rats.International journal of nephrology and renovascular disease · 2026Article
- Nanomedicine-Driven Precision Therapy for Renal Fibrosis: From Mechanistic Insights to Kidney-Targeted Interventions.International journal of nanomedicine · 2026Review
- Extracellular vesicles mediate immune regulation in acute kidney injury.Frontiers in immunology · 2026Review
- Decoding the ceRNA regulatory landscape: a comprehensive transcriptomic analysis of ncRNA-driven bladder fibrosis following spinal cord injury.Translational andrology and urology · 2025Article
- The role and therapeutic potential of exosome-mediated microRNAs regulatory networks in diabetic kidney disease.Molecular biology reports · 2025Review
- Extracellular Vesicles in Renal Inflammatory Diseases: Revealing Mechanisms of Extracellular Vesicle-Mediated Macrophage Regulation.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
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Abstract
In our investigation, we aimed to shed light on the role of senescent cells in renal fibrosis, considering the observed correlation between renal tubular epithelial cell senescence and the presence of renal fibrosis. Our findings confirm the manifestation of senescence characteristics in renal tubular epithelial cells during renal fibrosis and establish their capacity to trigger a transition from macrophages to myofibroblasts, known as macrophage-myofibroblast transition (MMT). Additionally, our study uncovered that extracellular vesicles released by senescent HK-2 cells (sHK-2) play a pivotal role in facilitating MMT. Subsequently, we investigated the miRNA profile in sHK-2-derived extracellular vesicles (sHK-2-EVs) and confirmed the elevated abundance of specific miRNAs, including miR-20a-5p and miR-21-5p, compared to normal HK-2-EVs. Notably, these miRNAs possess the capability to induce M2-like polarization in macrophages and enhance the expression of TGF-β. Moreover, TGF-β can stimulate macrophages to produce miR-20a-5p and miR-21-5p, establishing a positive feedback loop that amplifies the TGF-β/Smad pathway and facilitates the process of macrophage-myofibroblast transition.
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