TRPV2 channel inhibitors attenuate fibroblast differentiation and contraction mediated by keratinocyte-derived TGF-β1 in an in vitro wound healing model of rats

The wound healing process in skin proceeds sequentially in three phases, namely, inflammation, proliferation, and scar maturation, and involves sequential interactions of different cell types [1]. In granulation tissue, fibroblasts called myofibroblasts [1,2] obtain a contractile phenotype through the expression of α-smooth muscle actin (α-SMA) [3,4]. Such differentiation of dermal fibroblasts is believed to be involved in pathogenic scarring and fibrosis [5]. Thus, pharmacological intervention in the differentiation of fibroblasts may be beneficial for the prevention of hypertrophic scar formation and contractures.