Journal
SCIENTIFIC REPORTS
Volume 7, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/srep43446
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Funding
- Special Research Fund of Ministry of Health for Non-Profit Sector [201302010]
- Major National Projects for Infectious Diseases [2012ZX10002007]
- National Basic Research Program of China [2012CB519002]
- National Natural Science Foundation of China [81572047, 81570122]
- Program for Professor of Special Appointment (Eastern Scholar) at Shanghai Institutions of Higher Learning [QD2015005]
- Shanghai Municipal Education Commission-Gaofeng Clinical Medicine Grant Support [20161303]
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Although hepatitis B virus (HBV) infection is the leading cause of liver fibrosis (LF), the mechanisms underlying liver fibrotic progression remain unclear. Here, we investigated the gene expression profiles of HBV-related LF patients. Whole genome expression arrays were used to detect gene expression in liver biopsy samples from chronically HBV infected patients. Through integrative data analysis, we identified several pathways and key genes involved in the initiation and exacerbation of liver fibrosis. Weight gene co-expression analysis revealed that integrin subunit beta-like 1 (ITGBL1) was a key regulator of fibrogenesis. Functional experiments demonstrated that ITGBL1 was an upstream regulator of LF via interactions with transforming growth factor beta 1. In summary, we investigated the gene expression profiles of HBV-related LF patients and identified a key regulator ITGBL1. Our findings provide a foundation for future studies of gene functions and promote the development of novel antifibrotic therapies.
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