ArticleWorld journal of gastroenterology2017
M2-like Kupffer cells in fibrotic liver may protect against acute insult.
Article in World journal of gastroenterology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Single-cell transcriptomics reveals anti-inflammatory effects of prednisolone on the hepatic niche in biliary atresia.Scientific reports · 2026Article
- When Atrial Fibrillation Meets Alcoholic Liver Cirrhosis: Can Direct Oral Anticoagulants Bridge the Therapeutic Gap?Biomedicines · 2026Review
- Article
- Macrophage MerTK Promotes Liver Fibrosis in Nonalcoholic Steatohepatitis.Cell metabolism · 2020Article
- Phenotypic switch of human and mouse macrophages and resultant effects on apoptosis resistance in hepatocytes.Innate immunity · 2019Article
- Cellular Mechanisms of Hepatoprotection Mediated by M2-Like Macrophages.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the mechanism of hepatoprotection conferred by liver fibrosis through evaluating the activation phenotype of kupffer cells.
methodsControl and fibrotic mice were challenged with a lethal dose of D-GalN/lipopolysaccharide (LPS), and hepatic damage was assessed by histology, serum alanine transferase (ALT) levels, and hepatic expression of HMGB1, a potent pro-inflammatory mediator. The localization of F4/80 (a surrogate marker of KCs), HMGB1, and type I collagen (Col-1) was determined by immunofluorescence staining. The phenotype of KCs was characterized by real-time PCR. KCs isolated from control or fibrotic mice were challenged with LPS or HMGB1 peptide, and HMGB1 translocation was analyzed.
resultsLiver fibrosis protected mice against D-GalN/LPS challenge, as shown by improved hepatic histology and reduced elevation of ALT compared with the normal mice treated in the same way. This hepatoprotection was also accompanied by inhibition of HMGB1 expression in the liver. Co-localization of F4/80, HMGB1, and Col-1 was found in fibrotic livers, indicating the close relationship between KCs, HMGB1 and liver fibrosis. KCs isolated from fibrotic mice predominantly exhibited an M2-like phenotype.
conclusionM2-like Kupffer cells in fibrotic liver may exert a protective effect against acute insult by inhibiting the translocation of HMGB1.
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Registered trials
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