ArticleMediators of inflammation2026
Subchronic Alcohol Exposure Exacerbates Acetaminophen-Induced Acute Liver Injury via Macrophage-Mediated Inflammation and Mitochondrial Dysfunction.
Article in Mediators of inflammation, 2026. 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.
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Who cites it
1 citing paper in PubMed.
- Subchronic Alcohol Exposure Exacerbates Acetaminophen-Induced Acute Liver Injury via Macrophage-Mediated Inflammation and Mitochondrial Dysfunction.Mediators of inflammation · 2026Article
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Authors and funding
15 authors.
Funding
Abstract
Alcohol use is a major coexposure in patients taking acetaminophen (APAP), yet how subchronic alcohol exposure reshapes hepatic vulnerability to APAP remains incompletely defined. In this study, we examined the effects of chronic alcohol intake on APAP-induced liver injury in mice. Our results indicated that subchronic alcohol exposure significantly increased the mortality rate in APAP-overdosed mice. Alcohol pretreatment also exacerbated APAP-induced hepatic damage, as evidenced by elevated serum ALT and AST levels, enhanced inflammatory responses, and aggravated oxidative stress. Quantitative polymerase chain reaction (qPCR) analysis revealed that alcohol consumption suppressed mitochondrial biogenesis (MB)-related genes, including Pgc-1α and transcription factor A, mitochondrial (TFAM). Notably, macrophage depletion via clodronate liposomes not only attenuated hepatocyte injury and inflammation induction but also restored the expression of MB/function-related genes, including Pgc-1α, TFAM, and Opa1. These findings suggest macrophage-involved inflammatory amplification may aggravate APAP-induced liver injury, at least in part, by impairing mitochondrial adaptive repair responses.
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