ArticleJournal of gastroenterology and hepatology2025
Hepatic Inflammation and Liver Injury in a Model of Bacterial Infection Triggered Acute-on-Chronic Liver Injury.
Article in Journal of gastroenterology and hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- The JAK1 Inhibitor Upadacitinib Curbs Acute Liver Failure via Suppressing IFN-γ/JAK1/STAT1 and TNF-α/NF-κB/MAPK Pathways and Modulating Bax/Bcl-2 Ratio.Journal of xenobiotics · 2026Article
- A Nomogram Incorporating Sarcopenia and Nutritional Indicators for Mortality Prediction in HBV-Related Acute-Chronic Liver Failure.Healthcare (Basel, Switzerland) · 2026Article
- Hepatic Inflammation and Liver Injury in a Model of Bacterial Infection Triggered Acute-on-Chronic Liver Injury.Journal of gastroenterology and hepatology · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimAcute-on-chronic liver failure (ACLF) is characterized by acute decompensation of chronic liver disease in the presence of an acute trigger, and bacterial infection (BI) is the most common trigger of ACLF. Therefore, we aimed to establish a mouse model that mimics bacterial infection-related acute-on-chronic liver failure (BI-ACLF) to study the ongoing pathophysiological processes during disease progression.
methodsWild-type C57BL/6J (n = 12; wild-type, WT) and Abcb4
resultsHepatic cytokines and chemokines, monocyte chemoattractant protein-1 (Mcp-1), interleukins Il-2, Il-22, and regulated on activation, normal T-cell expressed and secreted (Rantes) were significantly upregulated in mice of KO-LPS groups compared to their counterparts. Induction of pyroptosis, apoptosis, and macrophage polarization towards the M1 phenotype was evident.
conclusionDifferential expression of hepatic cytokines and chemokines in Abcb4
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Registered trials
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