ArticleJHEP reports : innovation in hepatology2025
Temporal dichotomy of neutrophil function in acute liver injury and repair.
Article in JHEP reports : innovation in hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- uPAR-Targeting T Cell Engager Exerts Senolytic Effects in Mice and Non-Human Primates With Serum Aminotransferase Activity as a Safety Monitor.Aging cell · 2026Article
- Oxidative Stress and Alcohol-Related Hepatitis: A Role for Future Therapies.Antioxidants (Basel, Switzerland) · 2026Review
- Alternatively activated neutrophils limit T cell-driven neuroinflammation.Journal of neuroinflammation · 2026Article
- Integrated transcriptomic and phenotypic analyses reveal spatiotemporal variation in neutrophil Cd14 expression after hepatectomy.PloS one · 2026Article
- Spatial immune niche remodeling of the neutrophil-macrophage axis inchronic liver disease.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
24 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background & aims: Acetaminophen (APAP)-induced acute liver injury (APAP-ALI) is the leading cause of acute liver failure-induced death, with host innate immune responses driving outcomes. Neutrophils are activated and increased in APAP-ALI and reported to contribute to liver damage. However, neutrophil dysfunction in patients with acute liver failure is associated with non-survival, and recent reports highlight their importance in hepatic repair. Neutrophil-targeted therapies for APAP-ALI are hampered by this controversy and a lack of time-dependent investigation. Methods: Hepatic neutrophils were depleted at different times in a wild-type mouse model of APAP-ALI. Results: Neutrophils contributed both to hepatic damage and repair after APAP-ALI. Early liver necrosis was reduced by neutrophil depletion (34% to 23%, Conclusion: Recruited neutrophils contribute not only to hepatic damage early in APAP-ALI, but also to hepatic repair through a variety of pathways, including extracellular matrix remodeling, angiogenesis, hepatocyte proliferation, and promotion of an anti-inflammatory monocyte/macrophage phenotype. Impact and implications: Novel therapies are required for APAP-ALI to improve patient outcomes. Neutrophil products and functions are potential targets for future therapies, but current literature controversy and a lack of time-dependent studies hinder progression. This study resolves the literature controversy, showing that neutrophils have time-dependent dichotomous roles in APAP-ALI. These insights highlight that early neutrophil-targeted interventions to reduce liver damage could be detrimental to subsequent patient recovery. Therefore, future research should aim to either elucidate isolated damaging functions or harness reparative functions of neutrophils for late-stage novel therapies for APAP-ALI.
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Registered trials
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