ArticleMolecular medicine reports2019
Cathepsin S regulates renal fibrosis in mouse models of mild and severe hydronephrosis.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- A macrophage-induced subpopulation of mesenchymal cells expressing Fcer1g contributes to wound-induced fibrosis.Nature communications · 2026Article
- Proteomic insights into aprotinin's immunomodulatory effects in attenuating renal fibrosis in a unilateral ureteral obstruction model.Frontiers in immunology · 2026Article
- Phthalate exposure is associated with increased CVD risk in CKD: evidence from NHANES and network toxicology analysis.Renal failure · 2025Article
- Integrative Proteome- and Phenome-Wide Assessment Uncovers Causal Protein Drivers and Drug Targets for Heterogeneous Kidney Diseases.medRxiv : the preprint server for health sciences · 2025Article
- Cytokine priming enhances the antifibrotic effects of human adipose derived mesenchymal stromal cells conditioned medium.Stem cell research & therapy · 2024Article
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- Targeting ferroptosis: a new therapeutic opportunity for kidney diseases.Frontiers in immunology · 2024Review
- Title: Bioinformatic Identification of Genes Involved in Diabetic Nephropathy Fibrosis and their Clinical Relevance.Biochemical genetics · 2023Article
- Identification of immune-related molecular clusters and diagnostic markers in chronic kidney disease based on cluster analysis.Frontiers in genetics · 2023Article
- Piezo1 specific deletion in macrophage protects the progression of liver fibrosis in mice.Theranostics · 2023Article
- Cathepsin S inhibitor reduces high-fat-induced adipogenesis, inflammatory infiltration, and hepatic lipid accumulation in obese mice.Annals of translational medicine · 2022Article
- Inflammation-Driven Secretion Potential Is Upregulated in Osteoarthritic Fibroblast-Like Synoviocytes.International journal of molecular sciences · 2022Article
- Identifying effective diagnostic biomarkers and immune infiltration features in chronic kidney disease by bioinformatics and validation.Frontiers in pharmacology · 2022Article
- Identification of Hub Genes and Immune-Related Pathways for Membranous Nephropathy by Bioinformatics Analysis.Frontiers in physiology · 2022Article
- Proteomics changes after negative pressure wound therapy in diabetic foot ulcers.Molecular medicine reports · 2021Article
- Urine peptidome analysis in cardiorenal syndrome reflects molecular processes.Scientific reports · 2021Article
- The genetic background significantly impacts the severity of kidney cystic disease in the Pkd1Kidney international · 2021Article
- Decreased Expression of Canstatin in Rat Model of Monocrotaline-Induced Pulmonary Arterial Hypertension: Protective Effect of Canstatin on Right Ventricular Remodeling.International journal of molecular sciences · 2020Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a member of the cysteine protease family, cathepsin S (CTSS) serves an important role in diseases such as cancer, arthritis and atherosclerosis. Nevertheless, its role in renal fibrosis is unknown. In the present study, the effects of CTSS on renal fibrosis in mild (group M) and severe (group S) hydronephrosis were studied by reverse transcription‑-quantitative PCR (RT‑qPCR), western blot analysis (WB), Masson's trichrome staining and immunohistochemical staining in mouse models. The effects of CTSS on extracellular matrix (ECM) deposition and epithelial‑mesenchymal transition (EMT) and the potential mechanisms were further studied by RT‑qPCR and WB in transforming growth factor (TGF‑β1)‑stimulated TCMK‑1 cells. Compared with group N (no hydronephrosis), the expression levels of CTSS in the M and S groups were significantly higher, and a significant increase in ECM deposition was observed in the S group. In addition, compared with group N, the expression levels of TGF‑β1, α‑smooth muscle actin (α‑SMA), SMAD2, SMAD3, phosphorylated (p)SMAD2 and pSMAD3 in groups M and S were significantly higher, whereas the expression of E‑cadherin was significantly lower. Inhibition of CTSS expression increased the expression levels of TGF‑β1, α‑SMA, fibronectin, collagen‑I, SMAD2, SMAD3, pSMAD2 and pSMAD3, whereas E‑cadherin expression decreased. A significant increase in CTSS was observed in the TGF‑β1‑stimulated TCMK‑1 cell line. ECM deposition and EMT were also intensified. The opposite outcomes occurred after intervention with small interfering RNA targeting CTSS. In conclusion, CTSS affected EMT and the deposition of ECM. CTSS may mediate the regulation of fibrosis by the TGF‑β/SMAD signaling pathway. CTSS may serve an important role in the treatment of renal fibrosis.
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