Abstract
BACKGROUND AND AIM: Hepatic Stellate Cells (HSC) express α- and β-adrenoceptors and adrenergic inhibition results in reduced collagen I and α-smooth muscle actin (SMA) expression. Therefore, HSC were suggested to be the main cellular targets of sympathetic inhibition by β-blockers in experimental sinusoidal fibrosis. In order to study the role of the sympathetic nervous system in liver fibrogenesis we used the Abcb4 knock-out model developing non-HSC based, periportal fibrosis, which mimics primary sclerosing cholangitis (PSC).
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