| Literature DB >> 26998262 |
Ya-Lei Zhao1, Rong-Tao Zhu1, Yu-Ling Sun1.
Abstract
Liver fibrosis is the result of a sustained wound healing response to sustained chronic liver injury, which includes viral, alcoholic and autoimmune hepatitis. Hepatic regeneration is the dominant outcome of liver damage. The outcomes of successful repair are the replacement of dead epithelial cells with healthy epithelial cells, and reconstruction of the normal hepatic structure and function. Prevention of the development of epithelial-mesenchymal transition (EMT) may control and even reverse liver fibrosis. EMT is a critical process for an epithelial cell to undergo a conversion to a mesenchymal phenotype, and is believed to be an inflammation-induced response, which may have a central role in liver fibrosis. The origin of fibrogenic cells in liver fibrosis remains controversial. Numerous studies have investigated the origin of all fibrogenic cells within the liver and the mechanism of the signaling pathways that lead to the activation of EMT programs during numerous chronic liver diseases. The present study aimed to summarize the evidence to explain the possible role of EMT in liver fibrosis.Entities:
Keywords: fibrogenesis; hepatic stellate cells; liver fibrosis; myofibroblasts; transforming growth factor-β
Year: 2016 PMID: 26998262 PMCID: PMC4774315 DOI: 10.3892/br.2016.578
Source DB: PubMed Journal: Biomed Rep ISSN: 2049-9434