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CCN2 plays an important role in the pathogenesis of hypertrophic scars(HTSs)Although CCN2 is involved in many fibroproliferative events,the CCN2 induction signaling pathway in HTSs is yet to be elucidated Here,we first investigated the effect of the mitogenactivated protein kinases(MAPKs)on CCN2,induced a-smooth muscle actin(a-SMA)and collagen I expression in human HTS fibroblasts(HTSFs) Then we established HTSs 1n a rabbit ear model and determined the effect of MAPKs on the pathogenesis of HTSs MAPK pathways were activated by CCN2 in HTSFs Extracellular signalregulated kinase(ERK)and c-Jun N-terminal kinase(JNK)1nhibitors significantly 1nhibited CCN2-induced expression of a-SMA and collagen I 1n HTSFs In the rabbit ear model of the HTS.JN-K and ERK 1nhibitors significantly improved the architecture of the rabbit ear scar and reduced scar formation on the rabbit ear Our results 1ndicate that ERK and TNK mediate collagen I expression and scarring of the rabbit ear,and may be considered for specific drug therapy targets for HTSs Keywords Hypertrophic scar Extracellular signal-regulated kinase c-Jun N-terminal kinase.