ATP6AP2 and Myocardial fibrosis: Both PRR and AT1R activation have been shown to stimulate p38MAPK signaling (Stockand and Meszaros, 2003; Lee et al., 2004; Gao et al., 2016), making this pathway a critical node in the convergence of hemodynamic, hormonal, and inflammatory insults that promote myocardial fibrosis (Figure 3).