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<正>AngiotensinⅡis a powerful mediator to induce cardiac remodeling and fibrosis.Transforming growth factor-pi (TGF-β1) and extracellular signal-regulated kinase(ERK) have been implicated in the angiotensinⅡ-induced cardiac fibrosis. However,the signaling pathways for this angiotensinⅡeffect and the interaction between ERK and the TGF-β1 signaling in this effect have not been well-illustrated.Cardiac fibroblasts were prepared from the ventricles of adult male Sprague Dawley rats.They were treated with 1μM angiotensinⅡin the presence or absence of losartan(angiotensinⅡATI receptor antagonist),PD123319(angiotensinⅡAT2 receptor antagonist), an anti-TGF-β1 antibody or PD98059(ERK inhibitor). The cells were collected for Western blotting and reverse transcription -polymerase chain reaction.AngiotensinⅡcaused a significant increase of the expression of TGF-β1,ERK1,phosphorylated -Smad2/3,Smad4 and collagenⅠ.This increase was attenuated by losartan but was not affected by PD123319.An anti-TGF-β1 antibody and PD98059 diminished angiotensinⅡ-induced Smad2/3 phosphorylation and the expression of Smad7 and collagenⅠ.Our results suggest that angiotensinⅡinduces collagenⅠexpression through angiotensinⅡATI receptor-TGF-β1 -Smads signaling pathway in cardiac fibroblasts.ERK,by regulating Smads signaling,also participated in the angiotensinⅡ-induced collagenⅠexpression.