Hepatitis C virus (HCV) infection is currently the most common cause of fibrosing liver disease and represents a major clinical challenge. In patients with HCV infection, inflammation and injury lead to fibrosis and cirrhosis in a significant proportion of patients; cirrhosis in turn has multiple clinical sequelae. Therefore, understanding the pathological basis of fibrogenesis in hepatitis C infection is critical. This review will highlight fundamental issues underlying the fibrogenic response to injury and in addition will focus on potential points of intervention.
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Gene
November 2024
Department of Hepatobiliary-Pancreatic Surgery, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin, China. Electronic address:
Although antiviral drugs can effectively inhibit hepatitis B virus (HBV) replication, the maintenance of chronic inflammation in the liver is still considered to be an important cause for the progression of HBV-related liver disease to liver fibrosis and advanced liver disease. As an endogenous inhibitory receptor of IL-1R and TLR signaling pathways, single immunoglobulin interleukin-1-related receptor (SIGIRR) has been proven to reduce inflammation in tissues to maintain system homeostasis. However, the relationship between SIGIRR expression and HBV replication and inflammatory pathway activation in hepatocytes remains unclear.
View Article and Find Full Text PDFJ Clin Transl Hepatol
June 2024
Department of Cardiology, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Key Cardiovascular Specialty, Laboratory of Children's Important Organ Development and Diseases of Chongqing Municipal Health Commission, Chongqing, China.
Background And Aims: Hepatic fibrosis (HF) is a critical step in the progression of hepatocellular carcinoma (HCC). Gene associated with retinoid-IFN-induced mortality 19 (GRIM19), an essential component of mitochondrial respiratory chain complex I, is frequently attenuated in various human cancers, including HCC. Here, we aimed to investigate the potential relationship and underlying mechanism between GRIM19 loss and HF pathogenesis.
View Article and Find Full Text PDFEndocrinology
July 2024
The Centre for Diabetes, Obesity and Endocrinology Research (CDOER), The Westmead Institute for Medical Research, The University of Sydney, Sydney, NSW 2145, Australia.
Vitamin D signals through the vitamin D receptor (VDR) to induce its end-organ effects. Hepatic stellate cells control development of liver fibrosis in response to stressors and vitamin D signaling decreases fibrogenesis. VDR expression in hepatocytes is low in healthy liver, and the role of VDR in hepatocyte proliferation is unclear.
View Article and Find Full Text PDFJ Hepatol
November 2024
Division of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria; Christian-Doppler Laboratory for Portal Hypertension and Liver Fibrosis, Medical University of Vienna, Vienna, Austria; Center for Molecular Medicine (CeMM) of the Austrian Academy of Science, Vienna, Austria.
J Pathol
August 2024
Department of Medical Laboratory Science and Biotechnology, College of Health Sciences, Kaohsiung Medical University, Kaohsiung, Taiwan.
The relevance of aberrant serum IgG N-glycosylation in liver fibrosis has been identified; however, its causal effect remains unclear. Because hepatic stellate cells (HSCs) contribute substantially to liver fibrosis, we investigated whether and through which mechanisms IgG N-glycosylation affects the fibrogenic properties of HSCs. Analysis of serum IgG N-glycome from 151 patients with chronic hepatitis B or liver cirrhosis revealed a positive correlation between Ishak fibrosis grading and IgG with agalactosyl N-glycoforms on the crystallizable fragment (Fc).
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