ArticleVeterinary research2025
PEDV infection downregulates goblet cell differentiation through activating the Notch pathway.
Article in Veterinary research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The Interplay Between Autophagy and Porcine Epidemic Diarrhea Virus: From Molecular Mechanisms to Therapeutic Perspectives.Microorganisms · 2026Review
- Virus-Induced Intestinal Barrier Injury: Mechanisms and Therapeutic Perspectives.Veterinary sciences · 2026Review
- The Compound Terminalia Chebula Extract Alleviates PEDV-Induced Colonic Injury in Suckling Piglets by Enhancing Antioxidant Capacity, Suppressing Inflammation, Restoring Intestinal Function, and Inhibiting Viral Replication.Animals : an open access journal from MDPI · 2026Article
- Cross-Talk Between Pyroptosis and Ferroptosis Promotes Intestinal Inflammation and Barrier Failure During PEDV Infection.Biomolecules · 2026Article
- Perspective: from pathogenesis to treatment in veterinary science through organoid disease modelling.Frontiers in veterinary science · 2026Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Porcine epidemic diarrhoea virus (PEDV) is the most widespread porcine coronavirus worldwide, causing high mortality and a high incidence rate among piglets. The molecular mechanisms by which PEDV regulates epithelial cell function and differentiation, as well as its disruption of the intestinal mucosal barrier, are not yet fully understood. This study reveals that PEDV infection reduces the number of goblet cells and impairs the intestinal barrier integrity in newborn piglets. Regarding the pathways involved in the differentiation of intestinal stem cells (ISCs), PEDV infection concurrently activates the Notch and MAPK pathways while suppressing the Wnt/β-catenin pathway in the intestines of piglets. Furthermore, in vitro experiments using intestinal monolayer organoid models showed that PEDV infection hinders goblet cell differentiation by activating the Notch signalling pathway. Additionally, the PEDV-encoded ORF3 protein, which is crucial for activating the Notch pathway, inhibits goblet cell differentiation in PEDV-infected intestinal monolayer organoids. This study offers new insights into the mechanisms underlying intestinal mucosal barrier dysfunction induced by PEDV infection.
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