Objective：To explore the possible pathways and regulatory mechanism of TGFβ1induced transdifferentiation of derma fibroblasts(FB) into myofibroblasts. Methods: Mice Wildtype and Smad3 knockout(Smad3 KO) derma FB were divided into 9 groups,namely,A:Wildtype FB; B:Wildtype FB+TGFβ1; C:Wildtype FB+SB431542; D:Wildtype FB+SB431542+TGFβ1; E:Smad3 KO FB; F:Smad3 KO FB+TGFβ1; G:Wildtype FB+SB203580+TGFβ1; H:Wildtype FB+PD98059+TGFβ1; and I:Wildtype FB+SP600125+TGFβ1. After synchronization treatment,the cells were treated with TGFβ1 with or without pretreatment with above mentioned kinases inhibitors. Then the cells were collected for RNA extraction and the expression of αSMA was detected by real time quantitative RTPCR; some cells were analyzed by single cell RTPCR to test the positive expression rate of αSMA.Results: The expression and positive rate of αSMA in SB431542 group and Smad3 knockout group were significantly increased（group E vs. group A；group D vs. group C；group F vs. group E，P<0.01） and those in SP600125 group and SB203580 group were significantly inhibited（group G and I vs. group B，P<0.05）. Conclusion: In TGFβ1induced derma fibroblasts transdifferentiation into myofibroblasts,Smad3 pathway plays a negative regulatory role and p38/MAPK and JNK/MAPK pathway play a positive regulatory role.