ArticleFrontiers in pharmacology2025
Antagonizing IL-6 receptor restores pancreatic tissue resident NK cells activation and ameliorates pancreatic injury in the mouse model of MASH.
Article in Frontiers in pharmacology, 2025. 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.
- Expression characteristics of ferroptosis-related immune genes in chronic pancreatitis and screening and validation of key genes.BMC gastroenterology · 2026Article
- The central role of IL-6 in the differential effects of GLP-1 receptor agonists and metformin across multiple health conditions.Frontiers in immunology · 2026Review
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Authors and funding
7 authors.
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Abstract
Background and aim: Metabolic-associated steatohepatitis (MASH) and pancreatic inflammation are key complications of obesity-related metabolic syndrome. Elevated IL-6; a proinflammatory cytokine, contributes to liver steatosis and pancreatic β-islet cells dysfunction. This study explores pancreatic tissue-resident (tr)NK cells IL-6 receptor (IL-6R) in pancreatic injury in a murine MASH model. Methodology: MASH models were established using male Results: Conclusion: Our data highlights the importance of IL-6R modulation on trNK cells in remodeling pancreatic tissue after liver injury, emphasizing the liver-pancreas axis as a therapeutic target to prevent pancreatic damage, β-islet cells dysfunction and fibrosis and reduce the risk of diabetes and metabolic syndrome.
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