Evidence map›Paper›PMID 40287769›Full record

ArticleVirology journal2025

HBV activates hepatic stellate cells through RUNX2/ITGBL1 axis.

Fengchun Shi, Wei Tan, Wei Huang, Fei Ye, Mingjie Wang, Yongxiang Wang, Xinxin Zhang, Demin Yu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Virology journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. 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

8 authors.

Fengchun Shi *Department of Infectious Diseases, Research Laboratory of Clinical Virology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Wei Tan *Department of Infectious Diseases, Research Laboratory of Clinical Virology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Wei HuangDepartment of Gastroenterology, Affiliated Hospital of Nantong University, Nantong, 226000, China.
Fei YeDepartment of Infectious Diseases, Xiangya Hospital Central South University, Changsha, 410008, Hunan Province, China.
Mingjie WangDepartment of Gastroenterology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201821, China.
Yongxiang WangKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), Shanghai Frontier Science Center of Pathogenic Microorganisms and Infection, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai, China. yongxiangwang@fudan.edu.cn.ORCID 0000-0003-1405-7131
Xinxin ZhangDepartment of Infectious Diseases, Research Laboratory of Clinical Virology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China. zhangx@shsmu.edu.cn.ORCID 0000-0002-0598-6425
Demin YuDepartment of Infectious Diseases, Research Laboratory of Clinical Virology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China. ydm11367@rjh.com.cn.ORCID 0000-0001-9441-8616

Funding

2023 WBN Liver Fibrosis Research Foundation 2024029China Postdoctoral Science Foundation 2022M711719Shanghai Municipal Science and Technology Major Project ZD2021CY001
6 · The paper itself

Abstract

backgroundChronic hepatitis B (CHB) remains a global health challenge, with liver fibrosis serving as a critical determinant of disease progression. Despite antiviral treatments, liver fibrosis often persists in CHB patients, highlighting the need for additional biomarkers and therapeutic targets. This study investigates the molecular mechanism underlying HBV-induced liver fibrosis, focusing on the role of RUNX2 in regulating integrin beta-like 1 (ITGBL1), a key factor in fibrogenesis.

methodsWe examined the relationship between RUNX2 and ITGBL1 in both in vitro hepatocyte models and an in vivo HBV mouse model. Using chromatin immunoprecipitation (ChIP), luciferase reporter assays, and Western blotting, we assessed RUNX2 binding to the ITGBL1 promoter and its impact on gene expression. We also evaluated the effects of RUNX2 inhibition using Vitamin D3 and CADD522 on ITGBL1 expression and hepatic stellate cell activation.

resultsOur findings reveal that RUNX2 directly binds to the ITGBL1 promoter, enhancing its expression and promoting hepatic stellate cell activation. We show that HBV infection significantly upregulates both RUNX2 and ITGBL1 in liver cells. Inhibition of RUNX2 with Vitamin D3 or CADD522 significantly reduced ITGBL1 levels and blocked hepatic stellate cell activation. These results suggest that the RUNX2/ITGBL1 pathway is critical in the progression of liver fibrosis in HBV-infected patients.

conclusionsRUNX2 promotes liver fibrosis in HBV-infected patients by upregulating ITGBL1 expression. Our findings suggest that targeting RUNX2 could be a potential therapeutic approach to mitigate liver fibrosis in chronic hepatitis B.

Indexed as

Core Binding Factor Alpha 1 SubunitHepatic Stellate CellsHepatitis B, ChronicHepatitis B virusAnimalsDisease Models, AnimalHepatocytesHumansLiver CirrhosisMaleMiceMice, Inbred C57BLPromoter Regions, GeneticCore Binding Factor Alpha 1 SubunitRUNX2 protein, humanChronic hepatitis BITGBL1Liver fibrosisRUNX2

Identifiers

PMID40287769
PMCPMC12032756

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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.