Liver fibrosis: Pathophysiology and clinical implications

Liver fibrosis is a clinically significant finding that has major impacts on patient morbidity and mortality. The mechanism of fibrosis involves many different cellular pathways, but the major cell type involved appears to be hepatic stellate cells. Many liver diseases, including Hepatitis B, C, and fatty liver disease cause ongoing hepatocellular damage leading to liver fibrosis. No matter the cause of liver disease, liver-related mortality increases exponentially with increasing fibrosis. The progression to cirrhosis brings more dramatic mortality and higher incidence of hepatocellular carcinoma. Fibrosis can also affect outcomes following liver transplantation in adult and pediatric patients and require retransplantation. Drugs exist to treat Hepatitis B and C that reverse fibrosis in patients with those viral diseases, but there are currently no therapies to directly treat liver fibrosis. Several mouse models of chronic liver diseases have been successfully reversed using novel drug targets with current therapies focusing mostly on prevention of myofibroblast activation. Further research in these areas could lead to development of drugs to treat fibrosis, which will have invaluable impact on patient survival. This article is categorized under: Translational, Genomic, and Systems Medicine > Translational Medicine Models of Systems Properties and Processes > Organ, Tissue, and Physiological Models

Automated summary

Liver fibrosis is a significant finding impacting patient morbidity and mortality, primarily involving hepatic stellate cells. Various liver diseases cause hepatocellular damage leading to fibrosis, with progression to cirrhosis increasing liver-related mortality and hepatocellular carcinoma incidence. Despite treatments for Hepatitis B and C, there are currently no therapies directly targeting liver fibrosis, but research on novel drug targets could potentially improve patient survival.