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Objective   Myofibroblast transformation has been shown to be associated with the reactive oxygen species- (ROS-) producing enzyme NADPH oxidase (Nox4). Inhibition of transient receptor potential channel canonical type 3 (TRPC3) attenuates mitochondrial calcium handling and ROS production in the vasculature of hypertensive rats. However, it remains elusive whether TRPC3 regulates mitochondrial calcium and ROS production and participates in myofibroblast transdifferentiation during wound healing.Methods and Results   In this study, we demonstrated that activation of TRPC3 by transforming growth factor  β  (TGF β  (TGF α SMA). Inhibition of TRPC3 with its specific inhibitor, Pyr3, significantly decreased TGF β  (TGF α SMA). Inhibition of TRPC3 with its specific inhibitor, Pyr3, significantly decreased TGF β  (TGF β  (TGF Trpc3 −/−   mice exhibited significantly attenuated myofibroblast transdifferentiation, as demonstrated by decreased  α SMA). Inhibition of TRPC3 with its specific inhibitor, Pyr3, significantly decreased TGF β  (TGF β  (TGF Trpc3 −/−   mice exhibited significantly attenuated myofibroblast transdifferentiation, as demonstrated by decreased  Trpc3 +/+   mice. In addition,  Trpc3 −/−   mice exhibited significantly attenuated myofibroblast transdifferentiation, as demonstrated by decreasedConclusions   Our data indicate that TGF β 1-mediated activation of TRPC3 enhances mitochondrial calcium and ROS production, which promotes myofibroblast transdifferentiation and HTS formation. Inhibition of the TRPC3-mediated Nox4/pSmad2/3 pathway may be a useful strategy to limit HTS formation after injury. β  (TGF

Transient Receptor Potential Channel Canonical Type 3 Deficiency Antagonizes Myofibroblast Transdifferentiation In Vivo