Liver fibrosis: Pathophysiology and clinical implications
Citations Over TimeTop 1% of 2020 papers
Abstract
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: Metabolic Diseases > Molecular and Cellular Physiology.
Related Papers
- → Hepatic fibrosis: It is time to go with hepatic stellate cell-specific therapeutic targets(2018)197 cited
- → A Selective PPARγ Modulator Reduces Hepatic Fibrosis(2020)6 cited
- → Non-Invasively Distinguishing Progress of Liver Fibrosis by Visualizing Hepatic Platelet Derived Growth Factor Receptor-Beta Expression with an MRI Modality in Mice(2020)1 cited
- Effectiveness of saponins from Panax notoginseng against hepatic fibrosis(2007)
- → Research progress on the relationship between transforming growth factor-β1 and hepatic fibrosis(2017)