Evidence map›Paper›PMID 41493826›Full record

ArticleHepatology communications2026

Targeting fatty acid metabolism in hepatic macrophages mitigates acetaminophen-induced liver injury and promotes regeneration in mice.

Xiaoyong Jiang, Beng Wu, Liuyu Xie, Hao Li, Chen Chen, Panpan Huang, Xiaoyu Chen, Qian Zhu, Hua Wang, Chaojie Hu

Abstract read
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In one paragraph

Article in Hepatology communications, 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

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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.

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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

10 authors.

Xiaoyong JiangSchool of Pharmaceutic Science, Anhui Medical University, Hefei, China.
Beng WuSchool of Pharmaceutic Science, Anhui Medical University, Hefei, China.
Liuyu XieDivision of Life Science and Medicine, Department of Clinical Laboratory, First Affiliated Hospital of USTC, University of Science and Technology of China, Hefei, Anhui, China.
Hao LiDivision of Life Science and Medicine, Department of Clinical Laboratory, First Affiliated Hospital of USTC, University of Science and Technology of China, Hefei, Anhui, China.
Chen ChenSchool of Pharmaceutic Science, Anhui Medical University, Hefei, China.
Panpan HuangDivision of Life Science and Medicine, Department of Clinical Laboratory, First Affiliated Hospital of USTC, University of Science and Technology of China, Hefei, Anhui, China.
Xiaoyu ChenAnhui International Travel Health Care Center, Hefei, China.
Qian ZhuSchool of Pharmaceutic Science, Anhui Medical University, Hefei, China.
Hua WangDepartment of Oncology, the First Affiliated Hospital of Anhui Medical University, Hefei, China.
Chaojie HuDivision of Life Science and Medicine, Department of Clinical Laboratory, First Affiliated Hospital of USTC, University of Science and Technology of China, Hefei, Anhui, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAn overdose of acetaminophen (APAP) can cause severe liver injury and may even lead to death. However, the mechanisms that underlie APAP-induced liver injury (AILI) are not fully understood. The extensive liver necrosis resulting from APAP overdose aggravates the sterile inflammatory response by activating resident macrophages and recruiting various immune cells. Numerous studies have highlighted the crucial role of lipid metabolism in macrophage function. This study investigated fatty acid metabolism in hepatic macrophages and its impact on the progression of AILI.

methodsWe administered APAP intraperitoneally to C57/B6L mice to induce acute liver injury and studied lipid changes in hepatic macrophages. We treated hepacytes with APAP and collected the conditioned medium to stimulate macrophages. Moreover, we generated a myeloid-specific knockout of Fasn mice to validate the role of de novo lipogenesis in macrophages during AILI.

resultsWe stained liver tissue sections with Bodipy493/503 lipid dye and observed elevated lipid levels in hepatic macrophages after AILI. Mechanistically, HMGB1 released from necrotic hepatocytes increases FASN expression by activating the PI3K/AKT/sterol regulatory element-binding protein-1 (SREBP1) signaling pathway in macrophages. The enhanced de novo lipogenesis increased inflammatory factor expression in macrophages and facilitated their migratory ability. Conversely, myeloid-specific knockout of Fasn reduced the inflammatory response of macrophages and inhibited their chemotaxis in vivo and in vitro. Furthermore, either myeloid-specific knockout of Fasn or treatment with orlistat, a FASN inhibitor, notably improved liver necrosis and accelerated injury resolution following AILI in mice.

conclusionsOur findings suggest that targeting de novo lipogenesis in hepatic macrophages may represent a novel strategy for treating AILI.

Indexed as

AcetaminophenChemical and Drug Induced Liver InjuryFatty AcidsLiver RegenerationMacrophagesAnalgesics, Non-NarcoticAnimalsDisease Models, AnimalFatty Acid Synthase, Type IHepatocytesHMGB1 ProteinLipid MetabolismLipogenesisLiverMaleMiceAcetaminophenAnalgesics, Non-NarcoticFasn protein, mouseFatty AcidsFatty Acid Synthase, Type IHMGB1 ProteinHMGB1 protein, mouseSterol Regulatory Element Binding Protein 1acetaminophen-induced liver injurychemotaxisFASNHMGB1inflammationmacrophage

Identifiers

PMID41493826
PMCPMC12772497

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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.