ArticleJournal of the American Society of Nephrology : JASN2011
Smad3-mediated upregulation of miR-21 promotes renal fibrosis.
Article in Journal of the American Society of Nephrology : JASN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 224 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
224 citing papers in PubMed, 1 synthesis or guideline pooled it, 399 citations in OpenAlex.
- A systematic review of overlapping microRNA patterns in systemic sclerosis and idiopathic pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2017Pooled it
- Urinary sediment miRNAs reflect tubulointerstitial damage and therapeutic response in IgA nephropathy.BMC nephrology · 2017Trial
- MicroRNA-21 in glomerular injury.Journal of the American Society of Nephrology : JASN · 2015Trial
- Targeting MicroRNA-21 in Chronic Kidney Disease: Lessons from the Lademirsen Story.Medical sciences (Basel, Switzerland) · 2026Review
- Emerging Urinary Biomarkers and Innovative Technologies for the Early Detection and Personalized Management of Chronic Kidney Disease.International journal of molecular sciences · 2026Review
- Review
- The Role of Non-Coding RNAs in the Pathogenesis and Progression of Diabetic Kidney Disease.International journal of molecular sciences · 2026Review
- Chromatin remodeling and epigenetic regulation in chronic kidney disease.Frontiers in genetics · 2026Review
- TGF-β in chronic kidney disease: a controversy for decades.Frontiers in immunology · 2026Review
- Erythropoietin alleviate obstructive renal fibrosis by regulating immunity and inflammation through miR-21-5p/SPRY1/ERK1/2/NF-κB pathway inhibition.Frontiers in molecular biosciences · 2026Article
- Circulating microRNAs miR-21-5p, miR-23a-3p and miR-26a-5p reflect clinical and molecular features of aging.Scientific reports · 2025Article
- Unraveling Non-coding RNAs and dysregulation of TGF-β signalling in cardiorenal syndrome, a focused review for molecular and clinical applications.Molecular biology reports · 2025Review
- MicroRNAs in Systemic Sclerosis: Involvement in Disease Pathogenesis and Potential Use as Diagnostic Biomarkers and Therapeutic Targets.Biomedicines · 2025Review
- Molecular and Cellular Mediators of Renal Fibrosis in Lupus Nephritis.International journal of molecular sciences · 2025Review
- Smad3 Mediates Renal Fibrosis via GPX4-Dependent Ferroptosis.International journal of biological sciences · 2025Article
- Observational
- Potential Player of Platelet in the Pathogenesis of Cardiotoxicity: Molecular Insight and Future Perspective.Cardiovascular toxicology · 2024Review
- TGF‑β/Smad signaling in chronic kidney disease: Exploring post‑translational regulatory perspectives (Review).Molecular medicine reports · 2024Review
- Endoplasmic Reticulum Stress-Mediated Cell Death in Renal Fibrosis.Biomolecules · 2024Review
- MicroRNA-10 Family Promotes Renal Fibrosis through the VASH-1/Smad3 Pathway.International journal of molecular sciences · 2024Article
164 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TGF-β/Smad signaling plays a role in fibrogenesis, but therapies targeting TGF-β are ineffective in treating renal fibrosis. Here, we explored the therapeutic potential of targeting TGF-β-induced microRNA in the progression of renal fibrosis. Microarray analysis and real-time PCR revealed upregulation of miR-21 in tubular epithelial cells (TECs) in response to TGF-β. Lack of Smad3, but not lack of Smad2, prevented cells from upregulating miR-21 in response to TGF-β. In addition, Smad3-deficient mice were protected from upregulation of miR-21 and fibrosis in the unilateral ureteral obstruction model. In contrast, conditional knockout of Smad2 enhanced miR-21 expression and renal fibrosis. Furthermore, ultrasound-microbubble-mediated gene transfer of a miR-21-knockdown plasmid halted the progression of renal fibrosis in established obstructive nephropathy. In conclusion, these data demonstrate that Smad3, but not Smad2, signaling increases expression of miR-21, which promotes renal fibrosis. Inhibition of miR-21 may be a therapeutic approach to suppress renal fibrosis.
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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.