ArticlePloS one2020
Novel AXL-specific inhibitor ameliorates kidney dysfunction through the inhibition of epithelial-to-mesenchymal transition of renal tubular cells.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Molecular mechanisms, therapeutic strategies, and inter-organ fibrosis crosstalk of Gla proteins in cardiovascular disease.Communications biology · 2026Review
- Intercellular GAS6-AXL signaling triggers podocyte cuproptosis in acute kidney injury upstream regulated by CEBPD.PloS one · 2026Article
- Serum proteome analysis detects early molecular signatures of disease progression in IgA nephropathy.Clinical kidney journal · 2025Article
- Single-Cell RNA Sequencing Delineates Renal Anti-Fibrotic Mechanisms Mediated by TRPC6 Inhibition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Role and Mechanisms of Tyro3 in Podocyte Biology and Glomerular Disease.Kidney diseases (Basel, Switzerland) · 2024Review
- Drugs in Development to Treat IgA Nephropathy.Drugs · 2024Review
- Targeting AXL cellular networks in kidney fibrosis.Frontiers in immunology · 2024Article
- Axl regulated survival/proliferation network and its therapeutic intervention in mouse models of glomerulonephritis.Arthritis research & therapy · 2022Article
- Are Baseline Levels of Gas6 and Soluble Mer Predictors of Mortality and Organ Damage in Patients with Sepsis? The Need-Speed Trial Database.Biomedicines · 2022Article
- Purinergic P2Y2 and P2X4 Receptors Are Involved in the Epithelial-Mesenchymal Transition and Metastatic Potential of Gastric Cancer Derived Cell Lines.Pharmaceutics · 2021Article
- Mesangioproliferative Kidney Diseases and Platelet-Derived Growth Factor-Mediated AXL Phosphorylation.Kidney medicineArticle
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Authors and funding
4 authors.
Funding
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Abstract
Chronic kidney diseases affect more than 800 million people globally and remain a high unmet need. Various therapeutic targets are currently under evaluation in pre-clinical and clinical studies. Because the growth arrest specific gene 6 (Gas6)/AXL pathway has been implicated in the pathogenesis of kidney diseases, we generated a novel selective and potent AXL inhibitor, CH5451098, and we evaluated its efficacy and elucidated its mechanism in an NEP25 mouse model that follows the clinical course of glomerular nephritis. In this model, CH5451098 significantly ameliorated the excretion of urinary albumin and elevation of serum creatinine. Additionally, it also inhibited tubulointerstitial fibrosis and tubular damage. To elucidate the mechanism behind these changes, we analyzed the effect of CH5451098 against transforming growth factor β1 (TGFβ1) and Gas6, which is a ligand of AXL receptor, in NRK-52E renal tubular epithelial cells. CH5451098 inhibited epithelial-to-mesenchymal transition (EMT) caused by the synergistic effects of TGFβ1 and Gas6 in NRK-52E cells. This inhibition was also observed in NEP25 mice. Taken together, these results suggest that CH5451098 could ameliorate kidney dysfunction in glomerular nephritis by inhibiting EMT in tubular cells. These results reveal that AXL strongly contributes to the disease progression of glomerular nephritis.
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