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CCN2 plays an important role in the patho-genesis of hypertrophic scars (HTSs).Although CCN2 isinvolved in many fibroproliferative events, the CCN2induction signaling pathway in HTSs is yet to be eluci-dated.Here, we first investigated the effect of the mitogen-activated protein kinases (MAPKs) on CCN2-induceda-smooth muscle actin (a-SMA) and collagen Ⅰ expressionin human HTS fi broblasts (HTSFs).Then, we establishedHTSs in a rabbit ear model and determined the effect of MAPKs on the pathogenesis of HTSs.MAPK pathwayswere activated by CCN2 in HTSFs.Extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK)inhibitors significantly inhibited CCN2-induced expressionof a-SMA and collagen Ⅰ in HTSFs.In the rabbit earmodel of the HTS, JNKand ERK inhibitors significantlyimproved the architecture of the rabbit ear scar and reducedscar formation on the rabbit ear.Our results indicate that ERK and JNK mediate collagen Ⅰ expression and scarring of the rabbit ear, and may be considered for specific drug therapy targets for HTSs.