ArticleCurrent molecular medicine2026
Pancreatic Elastase Affects Liver Injury by Activating Proinflammatory Cytokines in Kupffer Cells via the JAK2/STAT3 Signaling Pathway.
Article in Current molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Liver dysfunction associated with severe acute pancreatitis: molecular mechanisms and clinical insights.Hepatobiliary surgery and nutrition · 2026Article
- Analysis of the association between the neutrophil-to-lymphocyte ratio (NLR) and liver injury complicating acute pancreatitis: a retrospective study.Frontiers in medicine · 2026Article
- Ferroptosis in Hypertriglyceridemic Acute Pancreatitis: Mechanisms and Therapeutic Implications.Journal of inflammation research · 2025Review
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Authors and funding
6 authors.
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Abstract
introductionThis study aimed to investigate the role of JAK2 (Janus kinase 2)/STAT3 (signal transducer and activator of transcription 3) signaling in liver injury during severe acute pancreatitis (SAP), focusing on pancreatic elastase- and lipopolysaccharide (LPS)-induced Kupffer cell (KC) activation.
methodsA rat SAP model was established via retrograde taurocholic acid infusion into the biliopancreatic duct. Inflammatory cytokine levels and JAK2/STAT3 pathway activity were quantified in liver tissues. KCs were treated with elastase/LPS ± AG490 (JAK2 inhibitor). Proinflammatory cytokines, RNA, and protein expression were analyzed. RESULTS AND DISCUSSION: SAP rats exhibited elevated TNF-α, IL-6, and IL-18 levels in both serum and liver tissues, with JAK2/STAT3 pathway activation. AG490 administration suppressed JAK2/STAT3 activation, reduced inflammation, and alleviated liver injury. Similarly, KCs treated with elastase and LPS showed increased proinflammatory cytokine levels and JAK2/STAT3 upregulation, which were mitigated by AG490 treatment.
conclusionThe findings highlighted the pivotal role of the JAK2/STAT3 signaling pathway in SAP-induced liver injury. Selective inhibition of this pathway by AG490 could reduce inflammation and protect against liver damage, suggesting its potential as a therapeutic target for inflammatory liver diseases.
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