ArticleJournal of advanced research2026
c-Myc-PANK3-EMT axis regulates the structure and function of intestinal barrier in ulcerative colitis.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Multiomics analyses revealed the roles of the epithelial-mesenchymal transition and novel early candidate diagnostic biomarkers in neonatal necrotising enterocolitis.Clinical and translational medicine · 2026Article
- Supplementation via DAF-16 andbioRxiv : the preprint server for biology · 2026Article
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Authors and funding
16 authors.
Funding
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Abstract
introductionThe repair of structural damage of the intestinal barrier is critical to rescue ulcerative colitis (UC), but there lacks effective targets currently.
objectivesThis study aims to explore mechanisms and identify potential targets for repairing the damaged intestinal barrier involved in UC.
methodsNontargeted metabolomic and transcriptomic analyses were utilized to characterize the metabolic features of DSS-induced colitis and identify potential therapeutic targets. Pantothenate kinase 3 (PANK3) was pharmacologically and genetically modulated to elucidate its mechanistic role. Chromatin immunoprecipitation and dual-luciferase reporter assays were employed to identify upstream regulators of PANK3, and PANK3 agonists were screened by high-throughput docking and further confirmed by in vitro and in vivo experiments.
resultsMetabolomic data indicated that perturbed metabolism involves pantothenate kinase. Clinical database, qPCR, WB, and immunohistochemical staining revealed a significant decrease of PANK3 in both patients and murine models of colitis. Pharmacological activation or overexpression of PANK3 restored the integrity of the intestinal barrier in UC mice, whereas PANK3 knockdown or inhibition exacerbated barrier dysfunction. PANK3 is negatively regulated by upstream c-Myc, and affects downstream, epithelial‒mesenchymal transition (EMT). In general, elevated c-Myc suppressed PANK3 transcription, promoted the EMT process and induced barrier disruption. The natural vitamin folic acid was identified as an agonist of PANK3, which could markedly improve the intestinal barrier in DSS-induced colitis.
conclusionThe c-Myc-PANK3-EMT axis plays a critical role in preserving the structure and function of intestinal barrier. PANK3 is a potential target and folic acid is a candidate agonist of PANK3 to repair intestinal barrier in UC.
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