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Seven Steps to Stellate Cells
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HBV activates hepatic stellate cells through RUNX2/ITGBL1 axis
Fengchun Shi1, Wei Tan1, Wei Huang2
1Department of Infectious Diseases, Research Laboratory of Clinical Virology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Virology Journal
|April 26, 2025
Summary
RUNX2 drives liver fibrosis in chronic hepatitis B (CHB) by increasing integrin beta-like 1 (ITGBL1) expression. Targeting RUNX2 may offer a new therapy for CHB patients with liver fibrosis.
Area of Science:
- Hepatology
- Molecular Biology
- Fibrosis Research
Background:
- Chronic hepatitis B (CHB) is a global health concern, with liver fibrosis significantly impacting disease progression.
- Existing antiviral therapies do not always resolve liver fibrosis in CHB patients, necessitating new biomarkers and treatments.
- This study explores the molecular mechanisms of HBV-induced liver fibrosis, specifically the role of RUNX2 in regulating ITGBL1.
Purpose of the Study:
- To investigate the molecular mechanism of HBV-induced liver fibrosis.
- To determine the role of RUNX2 in regulating ITGBL1 expression in the context of HBV infection.
- To assess the therapeutic potential of targeting the RUNX2/ITGBL1 pathway.
Main Methods:
- Utilized in vitro hepatocyte models and an in vivo HBV mouse model.
- Employed chromatin immunoprecipitation (ChIP), luciferase reporter assays, and Western blotting to analyze RUNX2-ITGBL1 interactions.
- Evaluated the impact of RUNX2 inhibition (using Vitamin D3 and CADD522) on ITGBL1 expression and hepatic stellate cell activation.
Main Results:
- RUNX2 was found to directly bind the ITGBL1 promoter, increasing its expression and promoting hepatic stellate cell activation.
- HBV infection led to significant upregulation of both RUNX2 and ITGBL1 in liver cells.
- Inhibition of RUNX2 effectively reduced ITGBL1 levels and inhibited hepatic stellate cell activation, indicating the pathway's critical role.
Conclusions:
- RUNX2 promotes liver fibrosis in HBV-infected patients through the upregulation of ITGBL1.
- Targeting RUNX2 presents a promising therapeutic strategy for managing liver fibrosis in chronic hepatitis B.
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