ReviewWorld journal of gastroenterology2025
Mechanistic insights into hepatic cell type-specific contributions to acetaminophen-induced acute liver injury.
Review in World journal of gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acetaminophen [N-acetyl-p-aminophenol (APAP)] overdose is a leading cause of acute liver failure worldwide, chiefly due to its hepatotoxic effects. The pathogenesis of APAP-induced acute liver injury (ALI) involves complex interactions among various hepatic cell types, each playing a distinct role in the progression of the injury. Hepatocytes, the primary targets of APAP toxicity, undergo oxidative stress, mitochondrial dysfunction, and necrosis following the formation of the toxic metabolite N-acetyl-p-benzoquinone imine. Additionally, other hepatic cells and infiltrating immune cells responding to liver injury significantly contribute to the pathogenesis of APAP-induced ALI. This review synthesizes current mechanistic insights to offer a detailed understanding of the specific contributions of hepatic cells to APAP-induced liver injury, emphasizing potential therapeutic targets designed to reduce liver damage and enhance patient outcomes. Additionally, it identifies potential therapeutic targets within these cellular pathways that could be leveraged to alleviate liver damage and enhance clinical outcomes for patients affected by APAP overdose.
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