ArticleJournal of cellular and molecular medicine2018
ASK1 inhibitor treatment suppresses p38/JNK signalling with reduced kidney inflammation and fibrosis in rat crescentic glomerulonephritis.
Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 58 citations in OpenAlex.
- Plasma proteome signatures of ASK1 inhibition by selonsertib associate with efficacy in the MOSAIC randomized trial for diabetic kidney disease.BMC nephrology · 2025Trial
- Contribution of p38 MAPK in liver fibrosis: An overview of mechanisms, signaling pathways, and therapeutic targets (Review).International journal of molecular medicine · 2026Review
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- [Research progress on the pathogenesis and clinical treatment of cirrhotic cardiomyopathy].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Review
- Crude saponin from Korean red ginseng alleviates di(2-ethylhexyl) phthalate-induced urogenital damage via regulating p38 MAPK/NF-κB signaling.Journal of ginseng research · 2025Article
- ASK1 inhibition by selonsertib attenuates elastase-induced emphysema in mice.Life sciences · 2025Article
- Exploring Neutrophil Heterogeneity and Plasticity in Health and Disease.Biomedicines · 2025Review
- Modulation of TGF-β signaling new approaches toward kidney disease and fibrosis therapy.International journal of biological sciences · 2025Review
- Synthesis and biological evaluation of quinoxaline derivatives as ASK1 inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2024Article
- CRLF1 bridges AKT and mTORC2 through SIN1 to inhibit pyroptosis and enhance chemo-resistance in ovarian cancer.Cell death & disease · 2024Article
- Aging, oxidative stress and degenerative diseases: mechanisms, complications and emerging therapeutic strategies.Biogerontology · 2023Review
- EP300 as a Molecular Integrator of Fibrotic Transcriptional Programs.International journal of molecular sciences · 2023Review
- Novel small-molecule compound VCP979 attenuates renal fibrosis in male rats with unilateral ureteral obstruction.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Article
- Deficiency of mindin reduces renal injury after ischemia reperfusion.Molecular medicine (Cambridge, Mass.) · 2022Article
- The role and regulation of apoptosis signal-regulated kinase 1 in liver disease.Molecular biology reports · 2022Review
- Regulation of the p38-MAPK pathway by hyperosmolarity and by WNK kinases.Scientific reports · 2022Article
- Selonsertib Enhances Kidney Protection Beyond Standard of Care in a Hypertensive, Secondary Glomerulosclerosis CKD Model.Kidney360 · 2022Article
- Advances in Immunosuppressive Agents Based on Signal Pathway.Frontiers in pharmacology · 2022Review
- Strategies for Improving Photodynamic Therapy Through Pharmacological Modulation of the Immediate Early Stress Response.Methods in molecular biology (Clifton, N.J.) · 2022Review
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of p38 mitogen-activated protein kinase (MAPK) and c-Jun amino terminal kinase (JNK) is prominent in human crescentic glomerulonephritis. p38 and JNK inhibitors suppress crescentic disease in animal models; however, the upstream mechanisms inducing activation of these kinases in crescentic glomerulonephritis are unknown. We investigated the hypothesis that apoptosis signal-regulating kinase 1 (ASK1/MAP3K5) promote p38/JNK activation and renal injury in models of nephrotoxic serum nephritis (NTN); acute glomerular injury in SD rats, and crescentic disease in WKY rats. Treatment with the selective ASK1 inhibitor, GS-444217 or vehicle began 1 hour before nephrotoxic serum injection and continued until animals were killed on day 1 (SD rats) or 14 (WKY rats). NTN resulted in phosphorylation (activation) of p38 and c-Jun in both models which was substantially reduced by ASK1 inhibitor treatment. In SD rats, GS-444217 prevented proteinuria and glomerular thrombosis with suppression of macrophage activation on day 1 NTN. In WKY rats, GS-444217 reduced crescent formation, prevented renal impairment and reduced proteinuria on day 14 NTN. Macrophage activation, T-cell infiltration and renal fibrosis were also reduced by GS-444217. In conclusion, GS-444217 treatment inhibited p38/JNK activation and development of renal injury in rat NTN. ASK1 inhibitors may have therapeutic potential in rapidly progressive glomerulonephritis.
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