TGFB1 and inflammatory response: However, the deletion of ENaC subunit reportedly causes decreased myogenic self-regulation, leading to renal inflammation and injury with elevated TGF-β1 and collagen III (Drummond et al., 2011), and in turn increased TGF-β1 can reduce ENaC functional activity in epithelial cells (Chang et al., 2008), implying that ENaC decreases in a positive feedback manner in response to renal injury.