Evidence map›Paper›PMID 42533544›Full record

ArticleJournal of gastroenterology and hepatology2026

Macrophage ACAT1 Aggravates Alcohol-Associated Liver Disease by Inducing Mitochondrial Damage and NLRP3 Activation.

Xi Zhao, Shiyu Peng, Keqing Zhong, Mingyue Wang, Huiling Cao, Shujun Ma, Jianni Qi, Yingchun Wang, Qiang Zhu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of gastroenterology and hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Xi ZhaoDepartment of Gastroenterology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.ORCID https://orcid.org/0009-0004-2766-9895
Shiyu PengDepartment of Gastroenterology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.
Keqing ZhongShandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Mingyue WangShandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Huiling CaoShandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Shujun MaUniversity Town Hospital, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, China.
Jianni QiShandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.ORCID https://orcid.org/0000-0002-9512-7762
Yingchun WangShandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Qiang ZhuDepartment of Gastroenterology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.ORCID https://orcid.org/0000-0002-5843-9724

Funding

National Natural Science Foundation of China 82370618National Natural Science Foundation of China 82570729Natural Science Foundation of Shandong Province ZR2023MH138Natural Science Foundation of Shandong Province ZR2024QH167Shandong Provincial Key Research and Development Program 2025KJHZ045
6 · The paper itself

Abstract

backgroundAlcohol-associated liver disease (ALD) is a major cause of advanced liver disease, with limited effective clinical interventions, highlighting an urgent need for new therapeutic targets. Acyl-CoA:cholesterol acyltransferase 1 (ACAT1) is a key cholesterol-metabolizing acyltransferase that catalyzes the esterification of free cholesterol into cholesteryl esters. It is highly expressed predominantly in macrophages and participates in the regulation of macrophage functions. Nevertheless, its role and underlying mechanism in alcoholic liver injury remain largely unclear.

resultsWe observed that co-stimulation with ethanol and LPS up-regulated ACAT1 expression, triggered inflammatory responses in macrophages, and aggravated liver function impairment, lipid deposition, and ROS accumulation in mice, thereby contributing to the progression of ALD. Mechanistically, ACAT1 upregulation induces mitochondrial damage and activates the NLRP3 inflammasome.

conclusionACAT1 is a positive regulatory factor in the inflammatory response of macrophages. It exacerbates ALD by inducing mitochondrial damage and activating NLRP3, providing a theoretical basis for the mechanism by which ACAT1 promotes ALD progression.

Indexed as

Acetyl-CoA C-AcetyltransferaseLiver Diseases, AlcoholicMacrophagesMitochondriaNLR Family, Pyrin Domain-Containing 3 ProteinAnimalsDisease ProgressionEthanolHumansInflammasomesMiceMice, Inbred C57BLReactive Oxygen SpeciesUp-RegulationAcetyl-CoA C-AcetyltransferaseEthanolInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseReactive Oxygen SpeciesACAT1alcohol‐related liver diseasemacrophagemitochondrial damageNLRP3

Identifiers

PMID42533544
PMCPMC13534283

What Socratic 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 Socratic graph.