Abstract
Background: Hepatic stellate cells (HSC) are the major source for extracellular matrix (ECM) production in liver fibrosis. Endoglin (ENG) is a type III auxiliary receptor for TGF-β that is expressed on HSCs. Due to different splicing there are two ENG isoforms, L- and S-Endoglin, which modulate TGF-β signaling differentially. TGF-β is the a profibrotic cytokine expressed in response to liver injury. This study analyzes the role of ENG and TGF-β signaling in two models of experimental liver fibrosis by cell line specific endoglin deletion in HSCs.
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