ArticleJHEP reports : innovation in hepatology2026
Epithelial MLCK deficiency alleviates alcohol-associated liver disease via dendritic-Th17 cell axis.
Article in JHEP reports : innovation in hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Perioperative gut microbial ecology: a new frontier for improving the prognosis of hepatocellular carcinoma surgery.Precision clinical medicine · 2026Review
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23 authors.
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Abstract
BACKGROUND &
aimsIntestinal dendritic cells (DCs) have a key role in immune regulation, especially during injury. The role of intestinal epithelial paracellular permeability in DC antigen presentation and its regulation is unclear although it is known that myosin light chain kinase (MLCK) regulates barrier permeability. Thus, we examined the role of MLCK in DC function and immune responses in alcohol-associated liver disease (ALD).
methodsWe used systemic and intestinal epithelial-specific Mylk-knockout models (n = 6 mice per group) to investigate the MLCK-mediated leak pathway in ALD. The effects of constitutively active MLCK in intestinal epithelial cells were also assessed (n = 6). Mechanistic investigations focused on LPA-LPAR2-Ca
resultsThe MLCK-mediated leak pathway was upregulated in ALD (n = 6, p <0.05). Both systemic and intestinal epithelial-specific Mylk knockout attenuated ALD progression, as evidenced by reduced liver injury markers (ALT decreased by 50%, n = 6, p <0.05), whereas constitutively active MLCK accelerated disease (n = 6, p <0.05). LPA-LPAR2 signaling activated MLCK via Ca
conclusionsThis study highlights the role of MLCK-regulated intestinal permeability in DC function and Th17 cell differentiation in ALD. Thus, targeting this pathway could provide new therapeutic strategies for ALD. IMPACT AND IMPLICATIONS: This study reveals the crucial role of MLCK-regulated intestinal paracellular permeability in ALD, expanding our understanding of the gut-liver interaction. The findings provide new insights into immune regulation and barrier function, offering potential therapeutic implications for the treatment of ALD. By highlighting the role of MLCK-mediated barrier function in DC function and Th17 cell differentiation, this research opens new avenues for clinical application, particularly in developing targeted therapies for ALD. For researchers, these findings offer a fresh perspective on the interplay between the gut microbiota and immune responses, advancing the field of immunology and gastrointestinal diseases.
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