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The noradrenergic system is proposed to play a prominent role in the pathogenesis of liver fibrosis. While α1and β-adrenergic receptors (ARs) are suggested to be involved in a multitude of profibrogenic actions, little is known about α2-AR-mediated effects and their expression pattern during liver fibrosis and cirrhosis. We explored the expression of α2-AR in two models of experimental liver fibrosis. We further evaluated the capacity of the α2-AR blocker mesedin to deactivate hepatic stellatedoi:10.18154/rwth-conv-242155 fatcat:n5ovh7jinza3xpfjw6rn2mikri