Evidence mapPaperPMID 42088639Full record

ArticleCell insight2026

Identification of Foxm1 as a critical regulator for metabolic dysfunction-associated steatotic liver disease by epigenomic and transcriptional profiling.

Chuanfei Zeng, Mingliang Wei, Huan Li, Fengyuan Niu, Ziqing Guo, Lian-Yun Li, Min Wu, Ming-Kai Chen

Abstract read
In one paragraph

Article in Cell insight, 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

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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

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

8 authors.

Chuanfei ZengDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, 430072, Hubei, China.
Mingliang WeiState Key Laboratory of Metabolism and Regulation in Complex Organisms, Frontier 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, 430072, Hubei, China.
Huan LiDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, 430072, Hubei, China.
Fengyuan NiuDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, 430072, Hubei, China.
Ziqing GuoDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, 430072, Hubei, China.
Lian-Yun LiState Key Laboratory of Metabolism and Regulation in Complex Organisms, Frontier 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, 430072, Hubei, China.
Min WuState Key Laboratory of Metabolism and Regulation in Complex Organisms, Frontier 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, 430072, Hubei, China.
Ming-Kai ChenDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, 430072, Hubei, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic regulation has emerged as a key mechanism in metabolic dysfunction-associated steatotic liver disease (MASLD). However, the systematic epigenomic profiling for MASLD progression is still lacking. To investigate the epigenetic mechanisms regulating MASLD, this study performed chromatin immunoprecipitation sequencing (ChIP-Seq) for H3K27ac, H3K4me1, H3K4me3, H3K9me3, and H3K27me3, along with transcriptomic profiling, using liver tissues from multiple stages of a Gubra-Amylin NASH (GAN) diet-induced mouse model. Transcriptomic analysis defined the 8- and 16-week time points as the inflammation stage, and the 20- and 24-week as the fibrosis stage. Chromatin state analysis revealed that enhancer and polycomb regions increase during MASLD progression. Differential enhancers were defined based on H3K27ac peaks, and Foxm1 was identified as a key transcription factor involved in MASLD.

Indexed as

EnhancerEpigenomicsFoxm1Lipid metabolismMASLD

Identifiers

PMID42088639
PMCPMC13137179

What Socratic holds

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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 Socratic graph.