Chrome Extension
WeChat Mini Program
Use on ChatGLM

HBV Activates Hepatic Stellate Cells Through RUNX2/ITGBL1 Axis

Virology Journal(2025)

Ruijin Hospital | Affiliated Hospital of Nantong University | Xiangya Hospital Central South University | Fudan University

Cited 0|Views1
Abstract
Chronic 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. We 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. Our 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. RUNX2 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.
More
Translated text
Key words
Chronic hepatitis B,RUNX2,ITGBL1,Liver fibrosis
PDF
Bibtex
AI Read Science
Must-Reading Tree
Example
Generate MRT to find the research sequence of this paper
Data Disclaimer
The page data are from open Internet sources, cooperative publishers and automatic analysis results through AI technology. We do not make any commitments and guarantees for the validity, accuracy, correctness, reliability, completeness and timeliness of the page data. If you have any questions, please contact us by email: report@aminer.cn
Chat Paper

要点】:本研究揭示了HBV通过RUNX2/ITGBL1轴激活肝星状细胞,促进肝脏纤维化的分子机制,并提出了以RUNX2为治疗靶点的潜在策略。

方法】:通过体外肝细胞模型、体内HBV小鼠模型以及ChIP、荧光素酶报告基因检测和Western印迹等方法,研究了RUNX2与ITGBL1的相互作用及其对基因表达的影响。

实验】:实验使用了Vitamin D3和CADD522抑制RUNX2,观察对ITGBL1表达和肝星状细胞激活的影响,发现抑制RUNX2能显著降低ITGBL1水平并阻止肝星状细胞激活,实验数据来源于肝细胞模型和HBV小鼠模型。