A high-salt diet promotes hypertrophic scarring through TRPC3-mediated mitochondrial Ca2+ homeostasis dysfunction

• DOI: 10.1016/j.heliyon.2023.e18629
• Publication Date: 2023-08-02T16:28:54Z
• Authors: Weijie Xia; Qianran Wang; Shaoyang Lin; Yuanyuan Wang; Junbo Zhang; Hailin Wang; Xia Yang; Yingru Hu; Huaping Liang; Yuangang Lu; Zhiming Zhu; Daoyan Liu
• Keywords: TRPC3; Transdifferentiation; Myofibroblast

Diet High in salt content have been associated with cardiovascular disease and chronic inflammation. We recently demonstrated that transient receptor potential canonical 3 (TRPC3) channels regulate myofibroblast transdifferentiation hypertrophic scars. Here, we examined how high activation of TRPC3 participates scarring during wound healing. In vitro, confirmed increased the protein expression marker alpha smooth muscle actin (α-SMA) wild-type mice (WT) primary cultured dermal fibroblasts but not Trpc3−/− mice. Activation by elevated cytosolic Ca2+ influx mitochondrial uptake a TRPC3-dependent manner. enhanced respiratory dysfunction excessive ROS production inhibiting pyruvate dehydrogenase action, activated ROS-triggered Rho kinase/MLC pathway WT vivo, persistent high-salt diet promoted collagen deposition Therefore, this study demonstrates enhances promotes scar formation through homeostasis, which activates ROS-mediated pMLC/pMYPT1 pathway. deficiency antagonizes diet-induced scarring. may be novel target for