ArticleScientific reports2017
The proteasome inhibitor bortezomib attenuates renal fibrosis in mice via the suppression of TGF-β1.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 44 citations in OpenAlex.
- Involvement of c-Myc/WWP1/TRIM65 Axis in Renal Fibrosis.Biomolecules · 2026Article
- Inhibitors of the ubiquitin‑proteasome system rescue cellular levels and ion transport function of pathogenic pendrin (SLC26A4) protein variants.International journal of molecular medicine · 2025Article
- Enzymatic post-translational modifications of proteins in chronic kidney disease: mechanisms, regulation, and clinical significance.Frontiers in pharmacology · 2025Review
- Regulation of myofibroblast dedifferentiation in pulmonary fibrosis.Respiratory research · 2024Review
- Bortezomib restrains M2 polarization and reduces CXCL16-associated CXCR6Molecular medicine (Cambridge, Mass.) · 2024Article
- APP-CD74 axis mediates endothelial cell-macrophage communication to promote kidney injury and fibrosis.Frontiers in pharmacology · 2024Article
- Targeting HSP47 and HSP70: promising therapeutic approaches in liver fibrosis management.Journal of translational medicine · 2022Review
- Bortezomib Inhibits Lung Fibrosis and Fibroblast Activation without Proteasome Inhibition.American journal of respiratory cell and molecular biology · 2022Article
- Bortezomib alleviates antibody-mediated rejection in kidney transplantation by facilitating Atg5 expression.Journal of cellular and molecular medicine · 2021Article
- Aristolochic acid I promoted clonal expansion but did not induce hepatocellular carcinoma in adult rats.Acta pharmacologica Sinica · 2021Article
- Aristolochic acid I induces impairment in spermatogonial stem cell in rodents.Toxicology research · 2021Article
- Tissue xanthine oxidoreductase activity in a mouse model of aristolochic acid nephropathy.FEBS open bio · 2021Article
- A Whole Genome-Wide Arrayed CRISPR Screen in Primary Organ Fibroblasts to Identify Regulators of Kidney Fibrosis.SLAS discovery : advancing life sciences R & D · 2020Article
- Oxidative Inactivation of the Proteasome Augments Alveolar Macrophage Secretion of Vesicular SOCS3.Cells · 2020Article
- Connectivity map-based drug repositioning of bortezomib to reverse the metastatic effect of GALNT14 in lung cancer.Oncogene · 2020Article
- Proteasome Inhibitors Bortezomib and Carfilzomib Stimulate the Transport Activity of Human Organic Anion Transporter 1.Molecular pharmacology · 2020Article
- Aristolochic Acid-Induced Nephrotoxicity: Molecular Mechanisms and Potential Protective Approaches.International journal of molecular sciences · 2020Review
- Protective Effects of Melatonin Against Aristolochic Acid-Induced Nephropathy in Mice.Biomolecules · 2019Article
- Bortezomib attenuates renal interstitial fibrosis in kidney transplantation via regulating the EMT induced by TNF-α-Smurf1-Akt-mTOR-P70S6K pathway.Journal of cellular and molecular medicine · 2019Article
- Dually Efficacious Medicine Against Fibrosis and Cancer.Medical sciences (Basel, Switzerland) · 2019Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kidney fibrosis and fibrogenesis significantly exacerbate chronic kidney disease (CKD) progression and are essential therapeutic targets. Bortezomib (BZM) is a proteasome inhibitor used for the treatment of multiple myeloma (MM). Several studies have demonstrated that BZM attenuates renal impairment in patients with MM, although this effect is generally considered to be the result of MM remission. Recently, several studies on BZM reported anti-fibrotic effects on liver and skin in experimental animal models. However, its effect on renal fibrosis has yet to be examined. Here, we investigated the anti-fibrotic effects of BZM in an experimental mouse model of fibrosis that uses aristolochic acid I (AA). Ten weeks of AA administration with BZM treatment twice a week significantly attenuated AA-induced renal dysfunction and albuminuria, reduced the expression of renal fibrosis-related proteins and kidney injury markers, such as αSMA, Kim1, and Ngal, and prevented renal fibrosis at the level of histopathology. Furthermore, pathological activation of TGFβ1-Smad3 signaling and apoptosis, essential pathophysiological causes of AA-induced nephropathy (AAN), were ameliorated by BZM, suggesting this mechanism may be involved in improving fibrosis in AAN. In conclusion, BZM directly inhibits renal fibrosis in CKD via suppression of TGFβ1-Smad3 signaling and is promising in terms of drug repositioning.
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