ArticleMedical science monitor : international medical journal of experimental and clinical research2018
Specific Inhibitor of Smad3 (SIS3) Attenuates Fibrosis, Apoptosis, and Inflammation in Unilateral Ureteral Obstruction Kidneys by Inhibition of Transforming Growth Factor β (TGF-β)/Smad3 Signaling.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 63 citations in OpenAlex.
- Protein mediators of chronic kidney disease in Type 2 diabetes: A mendelian randomization study.PLoS medicine · 2026Article
- Ablation of the renal tubular gluconeogenic enzyme PCK1 drives AKI-to-CKD transition by negatively regulating the TGF-β/Smad3 signaling pathway.Cellular and molecular life sciences : CMLS · 2026Article
- Review
- Paraxanthine and azilsartan attenuate gentamicin-induced renal fibrosis via modulation of TGF-β1/Smad3/7 signaling and miRNA-21/miRNA-200b expression.Journal of translational medicine · 2026Article
- Spatiotemporal Control of Intercellular Crosstalk: A New Therapeutic Paradigm for Halting Acute Kidney Injury to Chronic Kidney Disease Transition.Biomolecules · 2026Review
- Bioengineered exosome-mRNA hybrids: a breakthrough in targeted miRNA delivery for diabetic kidney fibrosis therapy.Frontiers in bioengineering and biotechnology · 2026Article
- Bone Marrow Mesenchymal Stem Cell Hydrogel-Mediated Fibroblast Reprogramming Restores Intestinal Function in Adhesive Small Bowel Obstruction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Fedratinib in chronic kidney disease: antifibrotic potential and renal safety signals from integrated network toxicology and pharmacovigilance.Renal failure · 2025Article
- Preclinical validation of TGFβ inhibitors as a novel therapeutic strategy for post-traumatic heterotopic ossification.Scientific reports · 2025Article
- Palmitate potentiates the SMAD3-PAI-1 pathway by reducing nuclear GDF15 levels.Cellular and molecular life sciences : CMLS · 2025Article
- Probing the binding hypothesis of Smad3 modulators by molecular dynamic simulations for Atherosclerosis Cardiovascular Disease (ASCVD).PloS one · 2025Article
- Differential regulation of MMP activity by TGFβ1 in fast- and slow- twitch muscle repair: insights from EDL and soleus muscle-derived myoblasts.Frontiers in cell and developmental biology · 2025Article
- Acetylation-regulated DUSP1 deficiency contributes to renal fibrosis progression.Theranostics · 2025Article
- ELABELA-derived peptide ELA13 attenuates kidney fibrosis by inhibiting the Smad and ERK signaling pathways.Journal of Zhejiang University. Science. B · 2024Article
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
- Therapeutic potential for renal fibrosis by targeting Smad3-dependent noncoding RNAs.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Review
- APC and ZBTB2 May Mediate M2 Macrophage Infiltration to Promote the Development of Renal Fibrosis: A Bioinformatics Analysis.BioMed research international · 2024Article
- Acne-induced pathological scars: pathophysiology and current treatments.Burns & trauma · 2024Review
- Obstructive nephropathy and molecular pathophysiology of renal interstitial fibrosis.Physiological reviews · 2023Review
- Specific inhibitor of Smad3 (SIS3) alleviated submandibular gland fibrosis and dysfunction after dominant duct ligation in mice.Journal of dental sciences · 2023Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Fibrosis is the common pathological feature in most kinds of chronic kidney disease (CKD). TGF-β/Smads signaling is the master pathway regulating kidney fibrosis pathogenesis, in which Smad3 acts as the integrator of various pro-fibrosis signals. In this study, we analyzed the role of SIS3, a specific inhibitor of Smad3, in mouse unilateral ureteral obstruction (UUO) kidneys. MATERIAL AND METHODS UUO mice were intraperitoneally injected with 0.2 mg/kg/day or 2 mg/kg/day of SIS3 or control saline for 7 days, followed by analysis of structure injury, fibrosis status, inflammation, apoptosis, and TGF-β/Smads signaling activity. RESULTS Our results indicated that SIS3 treatment dosage-dependently relieved the gross structure injury and tubular necrosis in UUO kidneys. Masson staining, immunohistochemistry, and real-time PCR showed significantly decreased extracellular matrix deposition, fibronectin staining intensity, and RNA levels of collagen I and collagen III in SIS3-treated UUO kidneys. SIS3 treatment also suppressed the activation of myofibroblasts, as evidenced by decreased expression levels of a-SMA and vimentin in UUO kidneys. The TGF-β/Smads signaling activity analysis showed that SIS3 inhibited the phosphorylation of Smad3 but not Smad2 and decreased the protein level of TGF-β1, suggesting specific inhibition of the TGF-β/Smad3 pathway in UUO kidneys. Furthermore, SIS3 treatment also ameliorated the increased pro-inflammatory TNF-α and COX2 in UUO kidneys and circulating IL-1β in UUO mice, and inhibited caspase-3 activity and the number of apoptotic cells. CONCLUSIONS SIS3 ameliorated fibrosis, apoptosis, and inflammation through inhibition of TGF-b/Smad3 signaling in UUO mouse kidneys.
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