Research Article
Transient Receptor Potential Channel Canonical Type 3 Deficiency Antagonizes Myofibroblast Transdifferentiation In Vivo
Figure 5
Schematic illustration depicting the mechanism by which enhanced TRPC3-mediated mitochondrial Ca2+ homeostasis and ROS generation contribute to myofibroblast transdifferentiation via the NOX4/pSmad pathway in the hypertrophic scars.