Evidence map›Paper›PMID 39956835›Full record

ArticleEpigenomics2025

Identification of IL-34 and Slc7al as potential key regulators in MASLD progression through epigenomic profiling.

Chuanfei Zeng, Mingliang Wei, Huan Li, Linxin Yu, Chuang Wang, Ziqi Mu, Ziyin Huang, Yujia Ke, Lian-Yun Li, Yong Xiao and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Epigenomics, 2025. 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. Review
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

12 authors.

Chuanfei ZengDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, China.
Mingliang WeiFrontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, College of Life Sciences, Taikang Center for Life and Medical Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, China.
Huan LiDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, China.
Linxin YuDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, China.
Chuang WangFrontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, College of Life Sciences, Taikang Center for Life and Medical Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, China.
Ziqi MuFrontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, College of Life Sciences, Taikang Center for Life and Medical Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, China.
Ziyin HuangDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, China.
Yujia KeDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, China.
Lian-Yun LiFrontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, College of Life Sciences, Taikang Center for Life and Medical Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, China.
Yong XiaoDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, China.
Min WuFrontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, College of Life Sciences, Taikang Center for Life and Medical Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, China.ORCID 0000-0003-1372-4764
Ming-Kai ChenDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveEpigenetic alterations are critical regulators in the progression of metabolic dysfunction-associated steatotic liver disease (MASLD); however, the dynamic epigenomic landscapes are not well defined. Our previous study found that H3K27ac and H3K9me3 play important roles in regulating lipid metabolic pathways in the early stages of MASLD. However, the epigenomic status in the inflammation stages still needs to be determined.

methodC57BL/6 male mice were fed with the methionine- and choline-deficient (MCD) or normal diet, and their serum and liver samples were collected after 6 weeks. Serum alanine aminotransferase (ALT), aspartate amino transferase (AST), total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) levels were measured. Chromatin immunoprecipitation sequencing (ChIP-Seq) for H3K27ac and H3K9me3 was performed together with RNA sequencing (RNA-seq) and key regulators were analyzed.

resultsThe target genes of enhancers with increased H3K27ac and decreased H3K9me3 signals are enriched in lipid metabolism and immuno-inflammatory pathways.

conclusionOur study reveals that active enhancers and heterochromatin associated with metabolic and inflammatory genes are extensively reprogrammed in MCD-diet mice, and

Indexed as

Epigenesis, GeneticFatty LiverInterleukinsAnimalsDisease ProgressionEpigenomicsHistonesLipid MetabolismMaleMiceMice, Inbred C57BLHistonesInterleukinsEpigenomicsH3K27acH3K9me3inflammationlipid metabolismmetabolic dysfunction-associated steatotic liver disease

Identifiers

PMID39956835
PMCPMC11970744

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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.