Evidence map›Paper›PMID 41645531›Full record

ArticleImmunity, inflammation and disease2026

MiR-18a-5p Attenuates Oxidative Stress and Inhibits Lipid Accumulation in Alcoholic Fatty Liver by Activating the CYP1A1-PPAR Axis.

XueMei Zhang, Wei Li, Ubaid Ullah, Ning Li, XinYu Geng, JiHan Qi, HongLiang Chen, Xu Zhang, Ying Hu, Lingling Yang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Immunity, inflammation and disease, 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

11 authors.

XueMei ZhangDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Wei LiDepartment of Gastroenterology, The First Affiliated Hospital of Jiamusi University, Jiamusi, China.
Ubaid UllahDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Ning LiDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
XinYu GengDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
JiHan QiDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
HongLiang ChenDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Xu ZhangDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Ying HuDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Lingling YangDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
ShiZhu JinDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.ORCID https://orcid.org/0000-0003-3613-0926

Funding

the Heilongjiang Natural Science Foundation Joint Guidance Project LH2023H036
6 · The paper itself

Abstract

backgroundLipid deposition in alcoholic fatty liver disease (AFL) represents an early stage in alcoholic liver disease progression and may contribute to carcinogenesis. MicroRNAs (miRNAs) play critical regulatory roles in liver biological processes.

methodsIn this study, we explored the miR-18a-5p/CYP1A1/PPAR axis in AFL using bioinformatics approaches. An AFL rat model was created, and second-generation sequencing identified differentially expressed mRNA in rat liver tissues. Core genes were identified through Gene Ontology, Kyoto Encyclopedia of Genes and Genomes pathway, and Gene Expression Omnibus database analyses. These genes were validated by qPCR in liver tissues and via in vitro experiments using L02 cells. The upstream miRNA identified in AFL was further verified in L02 cells using luciferase reporter assays.

resultsDifferential gene analysis revealed CYP1A1 and the PPAR pathway. In alcohol-induced L02 cells, increased CYP1A1 expression promoted oxidative stress and altered lipid metabolism via the PPAR pathway. MiR-18a-5p was identified as an upstream regulator that targets CYP1A1 to ameliorate alcohol-induced oxidative stress. Inhibition of CYP1A1 by miR-18a-5p improved the expression of PPARγ-related genes and decreased PPARα-related gene expression, thereby reducing lipid deposition.

conclusionThe miR-18a-5p/CYP1A1/PPAR axis is a novel pathway that could be targeted for AFL treatment.

Indexed as

Cytochrome P-450 CYP1A1Fatty Liver, AlcoholicLipid MetabolismMicroRNAsOxidative StressPeroxisome Proliferator-Activated ReceptorsPPAR alphaAnimalsCell LineDisease Models, AnimalHumansLiverMaleRatsSignal TransductionCytochrome P-450 CYP1A1MicroRNAsPeroxisome Proliferator-Activated ReceptorsPPAR alphaalcoholic fatty liver diseaseCYP1A1lipid metabolismmiR‐18a‐5pOxidative stressPPAR

Identifiers

PMID41645531
PMCPMC12877320

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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.