ArticlePloS one2013
Norcantharidin inhibits renal interstitial fibrosis by blocking the tubular epithelial-mesenchymal transition.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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
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Who cites it
18 citing papers in PubMed, 39 citations in OpenAlex.
- Norcantharidin attenuates amiodarone-induced pulmonary fibrosis via modulating miRNA-30a/GSK-3β/β-catenin and oxidative-inflammatory pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Synthesis, crystal structure and Hirshfeld surface analysis of (3aActa crystallographica. Section E, Crystallographic communications · 2026Article
- Mechanisms of norcantharidin against renal tubulointerstitial fibrosis.Pharmacological reports : PR · 2024Review
- Norcantharidin ameliorates the development of murine lupus via inhibiting the generation of IL-17 producing cells.Acta pharmacologica Sinica · 2022Article
- NCTD Prevents Renal Interstitial Fibrosis via Targeting Sp1/lncRNA Gm26669 Axis.International journal of biological sciences · 2021Article
- Protein Phosphatase 2A Inhibiting β-Catenin Phosphorylation Contributes Critically to the Anti-renal Interstitial Fibrotic Effect of Norcantharidin.Inflammation · 2020Article
- lncRNA MALAT1 mediated high glucose-induced HK-2 cell epithelial-to-mesenchymal transition and injury.Journal of physiology and biochemistry · 2019Article
- JianPi JieDu Recipe Inhibits Epithelial-to-Mesenchymal Transition in Colorectal Cancer through TGF-BioMed research international · 2017Article
- A High Content Screening Assay to Identify Compounds with Anti-Epithelial-Mesenchymal Transition Effects from the Chinese Herbal Medicine Tong-Mai-Yang-Xin-Wan.Molecules (Basel, Switzerland) · 2016Article
- Induced Pluripotent Stem Cells Inhibit Bleomycin-Induced Pulmonary Fibrosis in Mice through Suppressing TGF-β1/Smad-Mediated Epithelial to Mesenchymal Transition.Frontiers in pharmacology · 2016Article
- ATF6 pathway of unfolded protein response mediates advanced oxidation protein product-induced hypertrophy and epithelial-to-mesenchymal transition in HK-2 cells.Molecular and cellular biochemistry · 2015Article
- Article
- Norcantharidin inhibits renal interstitial fibrosis by downregulating PP2Ac expression.American journal of translational research · 2015Article
- Article
- Antifibrotic effects of KS370G, a caffeamide derivative, in renal ischemia-reperfusion injured mice and renal tubular epithelial cells.Scientific reports · 2014Article
- MicroRNA-328 inhibits renal tubular cell epithelial-to-mesenchymal transition by targeting the CD44 in pressure-induced renal fibrosis.PloS one · 2014Article
- Recent advances in renal interstitial fibrosis and tubular atrophy after kidney transplantation.Fibrogenesis & tissue repair · 2014Review
- Norcantharidin, derivative of cantharidin, for cancer stem cells.Evidence-based complementary and alternative medicine : eCAM · 2013Review
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (EMT) is thought to contribute to the progression of renal tubulointerstitial fibrosis. Norcantharidin (NCTD) is a promising agent for inhibiting renal interstitial fibrosis. However, the molecular mechanisms of NCTD are unclear. In this study, a unilateral ureteral obstruction (UUO) rat model was established and treated with intraperitoneal NCTD (0.1 mg/kg/day). The UUO rats treated with NCTD showed a reduction in obstruction-induced upregulation of α-SMA and downregulation of E-cadherin in the rat kidney (P<0.05). Human renal proximal tubule cell lines (HK-2) stimulated with TGF-β1 were treated with different concentrations of NCTD. HK-2 cells stimulated by TGF-β1 in vitro led to downregulation of E-cadherin and increased de novo expression of α-SMA; co-treatment with NCTD attenuated all of these changes (P<0.05). NCTD reduced TGF-β1-induced expression and phosphorylation of Smad2/3 and downregulated the expression of Snail1 (P<0.05). These results suggest that NCTD antagonizes tubular EMT by inhibiting the Smad pathway. NCTD may play a critical role in preserving the normal epithelial phenotype and modulating tubular EMT.
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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.