ArticleDrug design, development and therapy2015
Paclitaxel attenuates renal interstitial fibroblast activation and interstitial fibrosis by inhibiting STAT3 signaling.
Article in Drug design, development and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 66 citations in OpenAlex.
- Fibroblast Dynamics in Keloid Pathogenesis: Unraveling Cellular Crosstalk and Novel Therapeutic Targets.Dermatology research and practice · 2026Review
- Advances in the Targeted Drug Delivery System for Renal Fibrosis.International journal of nanomedicine · 2026Review
- CircERC1 facilitates chemoresistance through inhibiting pyroptosis and remodeling extracellular matrix in pancreatic cancer.Molecular cancer · 2025Article
- Plk1 promotes renal tubulointerstitial fibrosis by targeting autophagy/lysosome axis.Cell death & disease · 2023Article
- Prospects and Challenges of Electrospun Cell and Drug Delivery Vehicles to Correct Urethral Stricture.International journal of molecular sciences · 2022Review
- Genetic or siRNA inhibition of MBD2 attenuates the UUO- and I/R-induced renal fibrosis via downregulation of EGR1.Molecular therapy. Nucleic acids · 2022Article
- Methyl-CpG-binding domain protein 2 contributes to renal fibrosis through promoting polarized M1 macrophages.Cell death & disease · 2022Article
- Controlling Inflammation Pre-Emptively or at the Time of Cutaneous Injury Optimises Outcome of Skin Scarring.Frontiers in immunology · 2022Review
- Analysis of exosomal competing endogenous RNA network response to paclitaxel treatment reveals key genes in advanced gastric cancer.Frontiers in oncology · 2022Article
- Primary high-grade serous ovarian cancer cells are sensitive to senescence induced by carboplatin and paclitaxel in vitro.Cellular & molecular biology letters · 2021Article
- Apamin inhibits renal fibrosis via suppressing TGF-β1 and STAT3 signaling in vivo and in vitro.Journal of molecular medicine (Berlin, Germany) · 2021Article
- Review
- CircRNA_30032 promotes renal fibrosis in UUO model mice via miRNA-96-5p/HBEGF/KRAS axis.Aging · 2021Article
- Resistin induces cardiac fibroblast-myofibroblast differentiation through JAK/STAT3 and JNK/c-Jun signaling.Pharmacological research · 2021Article
- Puerarin Alleviates UUO-Induced Inflammation and Fibrosis by Regulating the NF-κB P65/STAT3 and TGFβ1/Smads Signaling Pathways.Drug design, development and therapy · 2021Article
- Paclitaxel Ameliorates Palmitate-Induced Injury in Mouse Podocytes.Medical science monitor basic research · 2020Article
- The Roles of Inflammation in Keloid and Hypertrophic Scars.Frontiers in immunology · 2020Review
- PARK2 promotes mitochondrial pathway of apoptosis and antimicrotubule drugs chemosensitivityTheranostics · 2020Article
- [Effect of low-concentration paclitaxel on collagen deposition outside rat pulmonary artery smooth muscle cells and related mechanism].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2019Article
- Targeting STAT3 signaling in kidney disease.American journal of physiology. Renal physiology · 2019Review
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Authors and funding
11 authors at 1 institution in 2 countries.
Funding
Abstract
Recent studies have demonstrated that paclitaxel might inhibit renal fibrosis. However, the underlying molecular mechanism remains unclear. In this study, we hypothesized that low-dose paclitaxel may block the STAT3 (signal transducer and activator of transcription 3) signaling to attenuate fibrosis in a mouse model with unilateral ureteral obstruction. Both NRK-49F cells and mice with unilateral ureteral obstruction were treated with paclitaxel. The results showed that paclitaxel treatment resulted in a dose- and time-dependent decrease in tyrosine-phosphorylated STAT3, and inhibited the expression of fibronectin, alpha-smooth muscle actin (α-SMA), and collagen I in cultured NRK-49F cells. S3I-201, an STAT3 inhibitor, also suppressed the expression of fibronectin, α-SMA, and collagen I in cultured NRK-49F cells. Mechanistically, paclitaxel treatment blocked the STAT3 activity by disrupting the association of STAT3 with tubulin and inhibiting STAT3 nucleus translocation. Furthermore, paclitaxel also ameliorated renal fibrosis by down-regulating the expression of fibronectin, α-SMA, and collagen I, and suppressed the infiltration of macrophages and production of TNF-α, IL-1β, TGF-β, and ICAM-1 (intercellular adhesion molecule 1) by inhibition of STAT3 activity in obstructive nephropathy. These results suggest that paclitaxel may block the STAT3 activity by disrupting the association of STAT3 with tubulin and inhibiting STAT3 nucleus translocation, consequently leading to the suppression of renal interstitial fibroblast activation and the development of renal fibrosis, and inhibition of proinflammatory cytokine production.
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