ArticleJournal of cellular and molecular medicine2019
Protease-activated receptor-1 contributes to renal injury and interstitial fibrosis during chronic obstructive nephropathy.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 38 citations in OpenAlex.
- Plasminogen Activation System and Fibroblasts: Impact on Tissue Remodeling, Disease, and Organ Homeostasis.Inflammation · 2026Review
- 4D Time-lapse imaging of cell dynamics in human alveolar tissue by label-free higher harmonic generation microscopy.Journal of translational medicine · 2026Article
- Serine proteases and protease-activated receptors signaling in the kidney.American journal of physiology. Cell physiology · 2025Review
- Review
- Observational
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- Role of protease-activated receptor 4 in mouse models of acute and chronic kidney injury.American journal of physiology. Renal physiology · 2024Article
- Interaction of estradiol and renin-angiotensin system with microRNAs-21 and -29 in renal fibrosis: focus on TGF-β/smad signaling pathway.Molecular biology reports · 2024Review
- Research progress on the mechanism of renal interstitial fibrosis in obstructive nephropathy.Heliyon · 2023Review
- Application of nanoparticles in the diagnosis and treatment of chronic kidney disease.Frontiers in medicine · 2023Review
- Baicalin protects against renal interstitial fibrosis in mice by inhibiting the TGF-β/Smad signalling pathway.Pharmaceutical biology · 2022Article
- Hirudin, a thrombin inhibitor, attenuates TGF-β-induced fibrosis in renal proximal tubular epithelial cells by inhibition of protease-activated receptor 1 expression via S1P/S1PR2/S1PR3 signaling.Experimental and therapeutic medicine · 2022Article
- Lack of miRNA-17 family mediates high glucose-induced PAR-1 upregulation in glomerular mesangial cells.Naunyn-Schmiedeberg's archives of pharmacology · 2022Article
- KLK8 promotes the proliferation and metastasis of colorectal cancer via the activation of EMT associated with PAR1.Cell death & disease · 2021Article
- Myeloid cell-derived coagulation tissue factor is associated with renal tubular damage in mice fed an adenine diet.Scientific reports · 2021Article
- Verbascoside alleviates renal fibrosis in unilateral ureteral obstruction rats by inhibiting macrophage infiltration.Iranian journal of basic medical sciences · 2021Article
- Poricoic acid A suppresses TGF-β1-induced renal fibrosis and proliferation via the PDGF-C, Smad3 and MAPK pathways.Experimental and therapeutic medicine · 2021Article
- Fibrosis in Chronic Kidney Disease: Pathogenesis and Consequences.International journal of molecular sciences · 2021Review
- Tissue factor cytoplasmic domain exacerbates post-infarct left ventricular remodeling via orchestrating cardiac inflammation and angiogenesis.Theranostics · 2021Article
- Dual blockade of protease-activated receptor 1 and 2 additively ameliorates diabetic kidney disease.American journal of physiology. Renal physiology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
End-stage renal disease, the final stage of all chronic kidney disorders, is associated with renal fibrosis and inevitably leads to renal failure and death. Transition of tubular epithelial cells (TECs) into mesenchymal fibroblasts constitutes a proposed mechanism underlying the progression of renal fibrosis and here we assessed whether protease-activated receptor (PAR)-1, which recently emerged as an inducer of epithelial-to-mesenchymal transition (EMT), aggravates renal fibrosis. We show that PAR-1 activation on TECs reduces the expression of epithelial markers and simultaneously induces mesenchymal marker expression reminiscent of EMT. We next show that kidney damage was reduced in PAR-1-deficient mice during unilateral ureter obstruction (UUO) and that PAR-1-deficient mice develop a diminished fibrotic response. Importantly, however, we did hardly observe any signs of mesenchymal transition in both wild-type and PAR-1-deficient mice suggesting that diminished fibrosis in PAR-1-deficient mice is not due to reduced EMT. Instead, the accumulation of macrophages and fibroblasts was significantly reduced in PAR-1-deficient animals which were accompanied by diminished production of MCP-1 and TGF-β. Overall, we thus show that PAR-1 drives EMT of TECs in vitro and aggravates UUO-induced renal fibrosis although this is likely due to PAR-1-dependent pro-fibrotic cytokine production rather than EMT.
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