ArticleClinical science (London, England : 1979)2022
WNT1-inducible signaling pathway protein 1 regulates kidney inflammation through the NF-κB pathway.
Article in Clinical science (London, England : 1979), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Molecular and neural circuit mechanisms of parvalbumin (PV) neurons in depression: Insights and advances.iScience · 2026Review
- Clinical Trial: Effects of Autologous Dendritic Cell Administration on Renal Hemodynamics and Inflammatory Biomarkers in Diabetic Kidney Disease.Diseases (Basel, Switzerland) · 2025Article
- An overview of CCN4 (WISP1) role in human diseases.Journal of translational medicine · 2024Review
- Comprehensive strategy for identifying extracellular vesicle surface proteins as biomarkers for chronic kidney disease.Frontiers in physiology · 2024Review
- Kidney tea [Frontiers in pharmacology · 2024Article
- Article
- CircUBXN7 promotes macrophage infiltration and renal fibrosis associated with the IGF2BP2-dependent SP1 mRNA stability in diabetic kidney disease.Frontiers in immunology · 2023Article
- Green Silver Nanoparticles Promote Inflammation Shutdown in Human Leukemic Monocytes.Materials (Basel, Switzerland) · 2022Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
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Abstract
Inflammation is a pathological feature of kidney injury and its progression correlates with the development of kidney fibrosis which can lead to kidney function impairment. This project investigated the regulatory function of WNT1-inducible signaling pathway protein 1 (WISP1) in kidney inflammation. Administration of recombinant WISP1 protein to healthy mice induced kidney inflammation (macrophage accrual and production of tumor necrosis factor α (TNF-α), CCL2 and IL-6), which could be prevented by inhibition of nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB). Furthermore, inhibition of WISP1, by gene knockdown or neutralising antibody, could inhibit cultured macrophages producing inflammatory cytokines following stimulation with lipopolysaccharides (LPSs) and kidney fibroblasts proliferating in response to TNFα, which both involved NF-κB signaling. Kidney expression of WISP1 was found to be increased in mouse models of progressive kidney inflammation-unilateral ureter obstruction (UUO) and streptozotocin (STZ)-induced diabetic nephropathy (DN). Treatment of UUO mice with WISP1 antibody reduced the kidney inflammation in these mice. Therefore, pharmacological blockade of WISP1 exhibits potential as a novel therapy for inhibiting inflammation in kidney disease.
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