Evidence map›Paper›PMID 40500691›Full record

ArticleMolecular cancer2025

Single-cell transcriptome reveals the reprogramming of immune microenvironment during the transition from MASH to HCC.

Yu Huang, Ying Xie, Yuqing Zhang, Zhemian Liu, Weihua Jiang, Yingying Ye, Jiale Tang, Zhenhua Li, Zhinan Yin, Xue-Jia Lin

Abstract read
In one paragraph

Article in Molecular cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. ApolipoproteinEiScience · 2026
    Article
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  3. Review
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  9. Article
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  11. The Role of CD4Cells · 2026
    Review
  12. Article
  13. Review
  14. A Mouse in vivo Model Mimicking MASH-Related HCC Pathogenesis.Journal of hepatocellular carcinoma · 2026
    Article
  15. Metabolic dysfunction and GZMKFrontiers in immunology · 2026
    Review
  16. Review
  17. Article
  18. Review
  19. 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

10 authors.

Yu Huang *The Affiliated Guangdong Second Provincial General Hospital of Jinan University, Jinan University, Guangzhou, 510317, China.
Ying Xie *The Affiliated Guangdong Second Provincial General Hospital of Jinan University, Jinan University, Guangzhou, 510317, China.
Yuqing ZhangThe Affiliated Guangdong Second Provincial General Hospital of Jinan University, Jinan University, Guangzhou, 510317, China.
Zhemian LiuThe Affiliated Guangdong Second Provincial General Hospital of Jinan University, Jinan University, Guangzhou, 510317, China.
Weihua JiangThe Affiliated Guangdong Second Provincial General Hospital of Jinan University, Jinan University, Guangzhou, 510317, China.
Yingying YeDepartment of Systems Biomedical Sciences, School of Medicine, Jinan University, Guangzhou, 510632, China.
Jiale TangSchool of Life Science and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou, 511436, China.
Zhenhua LiDepartment of Systems Biomedical Sciences, School of Medicine, Jinan University, Guangzhou, 510632, China. lizhenhua915@jnu.edu.cn.
Zhinan YinThe Affiliated Guangdong Second Provincial General Hospital of Jinan University, Jinan University, Guangzhou, 510317, China. tzhinan@jnu.edu.cn.
Xue-Jia LinThe Affiliated Guangdong Second Provincial General Hospital of Jinan University, Jinan University, Guangzhou, 510317, China. seta1988@126.com.

Funding

111 Project B16021Guangdong Major Project of Basic and Applied Basic Research 2023B0303000004National Key Research and Development Program of China 2020YFA0803502National Natural Science Foundation of China 32030036National Natural Science Foundation of China 32100695National Natural Science Foundation of China 82372797Pearl River S & T Nova Program of Guangzhou, China 201906010085Tip-top Scientific and Technical Innovative Youth Talents of Guangdong Special Support Program 2019TQ05Y110
6 · The paper itself

Abstract

backgroundThe immunological landscape of metabolic dysfunction-associated steatohepatitis (MASH)-driven hepatocellular carcinoma (HCC) is not well understood. Herein, we aim to delineate the immunological landscape in the MASH-to-HCC transition and to identify the critical genes that contribute to the pathogenesis of MASH-related HCC.

methodsA well-established MASH-driven HCC mouse model, STAM model, was first constructed. Thereafter, we applied single-cell RNA sequencing (scRNA-seq) analysis of CD45

resultsWe identified 23 major clusters corresponding to nine populations among 31,822 cells. Obviously, immunosuppressive and exhausted CD4

conclusionsWe illustrate the profound reprogramming of the liver immune microenvironment in the MASH-to-HCC transition and clarify the role of ApoE in MASH-driven HCC, implying that ApoE may serve as a potential therapeutic target for MASH-related HCC.

Indexed as

Carcinoma, HepatocellularFatty LiverLiver NeoplasmsSingle-Cell Gene Expression AnalysisTranscriptomeAnimalsApolipoproteins EB-LymphocytesCell DifferentiationCell LineageCellular ReprogrammingMaleMiceMice, Inbred C57BLT-LymphocytesApolipoproteins EApoEExhaustionImmunological landscapeImmunosuppressive microenvironmentMASH-to-HCC transition

Identifiers

PMID40500691
PMCPMC12153197

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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.