Year: 2023
Type: review
Abstract: Liver fibrosis of different etiologies is a serious health problem worldwide. There is no effective therapy available for liver fibrosis except the removal of the underlying cause of injury or liver transplantation. Development of liver fibrosis is caused by fibrogenic myofibroblasts that are not present in the normal liver, but rather activate from liver resident mesenchymal cells in response to chronic toxic or cholestatic injury. Many studies indicate that liver fibrosis is reversible when the causative agent is removed. Regression of liver fibrosis is associated with the disappearance of activated myofibroblasts and resorption of the fibrous scar. In this review, we discuss the results of genetic tracing and cell fate mapping of hepatic stellate cells and portal fibroblasts, their specific characteristics, and potential phenotypes. We summarize research progress in the understanding of the molecular mechanisms underlying the development and reversibility of liver fibrosis, including activation, apoptosis, and inactivation of myofibroblasts.
Language: English
Subfield: Hepatology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $2,750
Funders: National Research Foundation, Ministry of Education, National Research Foundation of Korea, National Institutes of Health, National Institute on Alcohol Abuse and Alcoholism, National Institute of Diabetes and Digestive and Kidney Diseases, National Institute of Environmental Health Sciences
Awards: DETECTION AND MODELS OF TOXICANT EXPOSURE, Novel IL-23 inhibitor for the treatment of alcohol associated liver disease, Development and validation of a novel 3D human in vitro model of nonalcoholic steatohepatitis to be used for novel therapeutic screening and research on disease mechanism., G6455692916, San Diego Digestive Diseases Research Center, The role of IL-17 signaling in alcohol-induced HCC, The Role of Portal Fibroblasts in Cholestatic Liver Fibrosis, Southern California Research Center for ALPD and Cirrhosis, Transcriptional co-regulators and macrophage gene expression, Epigenetics of human Hepatic Stellate Cells (HSCs) in NASH
OpenAlex ID: W4386969702