ArticleBMC nephrology2025
Study on effect of pancreatic kininogenase on diabetic nephropathy-induced fibrosis via Notch1/Hes1/Pten/Akt signaling pathway.
Article in BMC nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- The Role of Aryl Hydrocarbon Receptor-Dependent Signaling Pathway in the Profibrotic Effects of Dioxin-like Compounds in Human Renal Tubular Epithelial Cells.Environment & health (Washington, D.C.) · 2026Article
- Exploring the role of miR-126 in diabetes and its complications: a comprehensive review.Diabetology & metabolic syndrome · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
objectiveTo elucidate the mechanism by which pancreatic kininogenase (PKase) impacts renal fibrosis in diabetic nephropathy through modulation of the Notch1/Hes1 and Pten/Akt pathways.
methodsThis study employed in vivo models and cellular assays to investigate PKase's effects on cellular viability, apoptosis, and oxidative stress. Assay kits were used to assess these parameters, while protein expression levels were measured via Western Blot and RT-qPCR. Histological changes in kidney tissues were analyzed using HE and Masson's staining. Fibrosis markers-including E-cadherin, vimentin, α-SMA, Collagen I, TGF-β, and fibronectin-were evaluated through immunofluorescence and immunohistochemistry.
resultsAfter eight weeks of PKase treatment, significant improvements in blood glucose levels and associated symptoms were observed in diabetic nephropathy rats. Both in vivo and in vitro results demonstrated that PKase treatment inhibited the expression of diabetic nephropathy markers, including vimentin, α-SMA, FN, Collagen I, and TGF-β, while increasing the expression of E-cadherin. Additionally, the expression of Notch1, Hes1, and phosphorylated Akt (p-Akt) was upregulated, and Pten expression was suppressed, all of which were reversed by PKase treatment. Furthermore, both analyses indicated that PKase alleviated Jagged1-induced apoptosis and oxidative stress, and mitigated tubulointerstitial fibrosis.
conclusionPKase appears to ameliorate diabetic nephropathy-induced renal fibrosis by activating the Pten/Akt pathway and inhibiting the Notch1/Hes1 pathway, suggesting its potential as a therapeutic agent in diabetic nephropathy. CLINICAL TRIAL NUMBER: Not applicable.
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