ArticleScientific reports2025
Hepatitis B virus-infected hepatocytes promote the secretion of collagen VI to the extracellular matrix.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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.
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Who cites it
2 citing papers in PubMed.
- Immunomodulation by collagen VI across fibrotic and tumor microenvironmental contexts.Histology and histopathology · 2026Review
- Review
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Authors and funding
19 authors.
Funding
Abstract
Chronic hepatitis B virus (HBV) infection is a global health problem as it is the major cause of liver fibrosis and its complications cirrhosis and hepatocellular carcinoma. The role of virus-host interactions in liver fibrosis and progression to cancer remains poorly understood. Here we show that HBV infection of permissive cells trigger pathways relevant for extracellular matrix (ECM) remodeling, which is a hallmark of liver fibrosis. We demonstrate that collagen VI (ColVI) is secreted from infected cells and induces a profibrotic phenotype in patient-derived myofibroblasts and identified HBV-induced AKT signaling as a driver of ColVI expression in HBV-infected cells. Consistently, ColVI is upregulated in the liver of HBV patients with fibrosis. Our results suggest a role of ColVI as a driver of HBV-associated liver disease and highlight the potential of ColVI as a biomarker candidate and therapeutic target in HBV-infected patients.
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