ArticleCurrent medical science2022
Inhibition of Ubiquitin-specific Protease 4 Attenuates Epithelial-Mesenchymal Transition of Renal Tubular Epithelial Cells via Transforming Growth Factor Beta Receptor Type I.
Article in Current medical science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Deubiquitinase USP7 stabilizes the histone demethylase KDM5B and promotes the progression of renal fibrosis through the TSC1/mTOR axis.Molecular biomedicine · 2026Article
- The Ubiquitin-Specific Protease Family: Master Regulators of Renal Fibrosis Pathogenesis and Therapeutic Targets.International journal of molecular sciences · 2026Review
- Role of Ubiquitin-regulated EMT in Cancer Metastasis and Chemoresistance.International journal of biological sciences · 2025Review
- Crosstalk of ubiquitin system and non-coding RNA in fibrosis.International journal of biological sciences · 2024Review
- Ubiquitin-proteasome system as a target for anticancer treatment-an update.Archives of pharmacal research · 2023Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveUbiquitin-specific protease 4 (USP4) facilitates the development of transforming growth factor-beta 1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT) in various cancer cells. Moreover, EMT of renal tubular epithelial cells (RTECs) is required for the progression of renal interstitial fibrosis. However, the role of USP4 in EMT of RTECs remains unknown. The present study aimed to explore the effect of USP4 on the EMT of RTECs as well as the involved mechanism.
methodsIn established unilateral ureteral obstruction (UUO) rats and NRK-52E cells, immunohistochemistry and Western blot assays were performed.
resultsUSP4 expression was increased significantly with obstruction time. In NRK-52E cells stimulated by TGF-β1, USP4 expression was increased in a time-dependent manner. In addition, USP4 silencing with specific siRNA indicated that USP4 protein was suppressed effectively. Meanwhile, USP4 siRNA treatment restored E-cadherin and weakened alpha smooth muscle actin (α-SMA) expression, indicating that USP4 may promote EMT. After treatment with USP4 siRNA and TGF-β1 for 24 h, the expression of TGF-β1 receptor type I (TβRI) was decreased.
conclusionUSP4 promotes the EMT of RTECs through upregulating TβRI, thereby facilitating renal interstitial fibrosis. These findings may provide a potential target of USP4 in the treatment of renal fibrosis.
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