Evidence map›Paper›PMID 40271687›Full record

ArticleeLife2025

A host enzyme reduces metabolic dysfunction-associated steatotic liver disease (MASLD) by inactivating intestinal lipopolysaccharide.

Zhiyan Wang, Nore Ojogun, Yiling Liu, Lu Gan, Zeling Xiao, Jintao Feng, Wei Jiang, Yeying Chen, Benkun Zou, ChengYun Yu and 8 more

Abstract read
In one paragraph

Article in eLife, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Review
  2. Article
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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

18 authors.

Zhiyan WangDepartment of Immunology, School of Basic Medical Sciences, Department of Trauma-Emergency & Critical Care Medicine, Shanghai Fifth People's Hospital, Fudan University, Shanghai, China.
Nore OjogunInfectious Disease Division, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, United States.
Yiling LiuDepartment of Immunology, School of Basic Medical Sciences, Department of Trauma-Emergency & Critical Care Medicine, Shanghai Fifth People's Hospital, Fudan University, Shanghai, China.
Lu GanDepartment of Immunology, School of Basic Medical Sciences, Department of Trauma-Emergency & Critical Care Medicine, Shanghai Fifth People's Hospital, Fudan University, Shanghai, China.
Zeling XiaoDepartment of Immunology, School of Basic Medical Sciences, Department of Trauma-Emergency & Critical Care Medicine, Shanghai Fifth People's Hospital, Fudan University, Shanghai, China.
Jintao FengDepartment of Immunology, School of Basic Medical Sciences, Department of Trauma-Emergency & Critical Care Medicine, Shanghai Fifth People's Hospital, Fudan University, Shanghai, China.
Wei JiangDepartment of Rheumatology and Immunology, the Affiliated Hospital of Guizhou Medical University, Guizhou, China.
Yeying ChenDepartment of Immunology, School of Basic Medical Sciences, Department of Trauma-Emergency & Critical Care Medicine, Shanghai Fifth People's Hospital, Fudan University, Shanghai, China.
Benkun ZouBeiGene Institute, BeiGene (Shanghai) Research and Development Co., Ltd, Shanghai, China.
ChengYun YuDepartment of Immunology, School of Basic Medical Sciences, Department of Trauma-Emergency & Critical Care Medicine, Shanghai Fifth People's Hospital, Fudan University, Shanghai, China.
Changshun LiDepartment of Immunology, School of Basic Medical Sciences, Department of Trauma-Emergency & Critical Care Medicine, Shanghai Fifth People's Hospital, Fudan University, Shanghai, China.
Asha AshuoDepartment of Medical Microbiology and Parasitology, MOE/NHC/CAMS Key Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Xiaobo LiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Mingsheng FuDepartment of Gastroenterology, Shanghai Fifth People's Hospital, Fudan University, Shanghai, China.
Jian WuDepartment of Medical Microbiology and Parasitology, MOE/NHC/CAMS Key Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Yiwei ChuDepartment of Immunology, School of Basic Medical Sciences, Department of Trauma-Emergency & Critical Care Medicine, Shanghai Fifth People's Hospital, Fudan University, Shanghai, China.
Robert S MunfordInfectious Disease Division, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, United States.ORCID https://orcid.org/0000-0003-1509-1294
Mingfang LuDepartment of Immunology, School of Basic Medical Sciences, Department of Trauma-Emergency & Critical Care Medicine, Shanghai Fifth People's Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0002-8612-3444

Funding

Studies of the capsular-like antigen of F. tularensisP01AI044642 · NIAID · UNIVERSITY OF IOWA · PI NAUSEEF, WILLIAM M. · 1999 to 2014
$18.2M
INTERACTIONS OF ENDOTOXIN WITH PLASMA AND CELLSR01AI018188 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI VARLEY, ALAN WAYNE · 1985 to 2011
$3.9M
INTERACTIONS OF ENDOTOXIN WITH PLASMA AND CELLSR37AI018188 · NIAID · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI MUNFORD, ROBERT S · 1992 to 2001
$729k
Interactions of Endotoxin with Plasma and CellsR56AI018188 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI MUNFORD, ROBERT S · 2007 to 2007
$523k
Guizhou Provincial Science and Technology Department ZK2024 - 240National Natural Science Foundation of China 31570910National Natural Science Foundation of China 31770993National Natural Science Foundation of China 32170929National Natural Science Foundation of China 32260189National Natural Science Foundation of China 32300772National Natural Science Foundation of China 32370979National Natural Science Foundation of China 82301980National Natural Science Foundation of China 91742104NIAID NIH HHS P01 AI044642NIAID NIH HHS R01 AI018188NIAID NIH HHS R37 AI018188NIAID NIH HHS R56 AI018188NIH HHS AI18188NIH HHS AI44642Science and Technology Program of Guizhou Province gzwkj2023-568Shanghai Committee of Science and Technology 21ZR1405400
6 · The paper itself

Abstract

The incidence of metabolic dysfunction-associated steatotic liver disease (MASLD) has been increasing worldwide. Since gut-derived bacterial lipopolysaccharides (LPS) can travel via the portal vein to the liver and play an important role in producing hepatic pathology, it seemed possible that (1) LPS stimulates hepatic cells to accumulate lipid, and (2) inactivating LPS can be preventive. Acyloxyacyl hydrolase (AOAH), the eukaryotic lipase that inactivates LPS and oxidized phospholipids, is produced in the intestine, liver, and other organs. We fed mice either normal chow or a high-fat diet for 28 weeks and found that

Indexed as

Carboxylic Ester HydrolasesFatty LiverIntestinesLipopolysaccharidesAnimalsDiet, High-FatLipid MetabolismLiverMaleMiceMice, Inbred C57BLMice, Knockoutacyloxyacyl hydrolaseCarboxylic Ester HydrolasesLipopolysaccharidesacyloxyacyl hydrolasegut–liver axishumanimmunologyinflammationlipopolysaccharidemetabolic dysfunction-associated steatotic liver diseasemousesterol regulatory element-binding protein 1

Identifiers

PMID40271687
PMCPMC12021412

What OpenQuestion holds

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Registered trials

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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.