Evidence map›Paper›PMID 42605725›Full record

ArticleMediators of inflammation2026

Subchronic Alcohol Exposure Exacerbates Acetaminophen-Induced Acute Liver Injury via Macrophage-Mediated Inflammation and Mitochondrial Dysfunction.

Qingyang Zhang, Hu Liu, Weigao Zhang, Huiling Zhou, Yunfeng Zhu, Jiayi Xu, Xuening Ma, Kadierya Kuerban, Yong Huang, Lingna Qiu and 5 more

Abstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

Qingyang ZhangSchool of Environmental and Biological Engineering, Nanjing University of Science and Technology, 200 Xiaolingwei Street, Nanjing 210094, China, njust.edu.cn.ORCID https://orcid.org/0009-0006-2521-5245
Hu LiuSchool of Environmental and Biological Engineering, Nanjing University of Science and Technology, 200 Xiaolingwei Street, Nanjing 210094, China, njust.edu.cn.
Weigao ZhangSchool of Environmental and Biological Engineering, Nanjing University of Science and Technology, 200 Xiaolingwei Street, Nanjing 210094, China, njust.edu.cn.
Huiling ZhouSchool of Environmental and Biological Engineering, Nanjing University of Science and Technology, 200 Xiaolingwei Street, Nanjing 210094, China, njust.edu.cn.
Yunfeng ZhuSchool of Environmental and Biological Engineering, Nanjing University of Science and Technology, 200 Xiaolingwei Street, Nanjing 210094, China, njust.edu.cn.
Jiayi XuSchool of Environmental and Biological Engineering, Nanjing University of Science and Technology, 200 Xiaolingwei Street, Nanjing 210094, China, njust.edu.cn.
Xuening MaSchool of Environmental and Biological Engineering, Nanjing University of Science and Technology, 200 Xiaolingwei Street, Nanjing 210094, China, njust.edu.cn.
Kadierya KuerbanSchool of Environmental and Biological Engineering, Nanjing University of Science and Technology, 200 Xiaolingwei Street, Nanjing 210094, China, njust.edu.cn.
Yong HuangSchool of Environmental and Biological Engineering, Nanjing University of Science and Technology, 200 Xiaolingwei Street, Nanjing 210094, China, njust.edu.cn.
Lingna QiuSchool of Environmental and Biological Engineering, Nanjing University of Science and Technology, 200 Xiaolingwei Street, Nanjing 210094, China, njust.edu.cn.
Fei HeDepartment of Emergency Medicine, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, China, nju.edu.cn.ORCID https://orcid.org/0000-0003-3721-198X
Yiwen WengInternal Medicine Department, Chengdu Jinniu District People's Hospital, Chengdu, China.
Na FuDepartment of Traditional and Western Medical Hepatology, Third Hospital of Hebei Medical University, 139 Ziqiang Road, Shijiazhuang, Hebei, 050051, China, hebmu.edu.cn.ORCID https://orcid.org/0009-0006-2071-6307
Shao DaResearch Center of Translational Medicine, Shanghai Children's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200062, China, sjtu.edu.cn.
Dan WengSchool of Environmental and Biological Engineering, Nanjing University of Science and Technology, 200 Xiaolingwei Street, Nanjing 210094, China, njust.edu.cn.ORCID https://orcid.org/0000-0001-8078-6864

Funding

Chengdu Medical Research Project 2024242National Key Research and Development Program of China 2024YFF0619500National Natural Science Foundation of China 22376100National Natural Science Foundation of China 31970897National Natural Science Foundation of China 32100828
6 · The paper itself

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.

Indexed as

AcetaminophenChemical and Drug Induced Liver InjuryEthanolInflammationMacrophagesMitochondriaAnimalsLiverMaleMiceMice, Inbred C57BLOxidative StressPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaAcetaminophenEthanolPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseacetaminophenalcoholinflammationmacrophageoxidative stress

Identifiers

PMID42605725
PMCPMC13479109

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.