FGF18 and Myocardial fibrosis: However, FGFR3 knockdown abolished the cardioprotective effects of FGF18 compared with those FGF18-treated mice after TAC, including cardiomyocyte size (Supplementary Fig. 6a), myocardial fibrosis (Supplementary Fig. 6b), hydroxyproline content (Supplementary Fig. 6c) and cardiac function (Supplementary Fig. 6d, Supplementary Table 3), as well as promoting the accumulation of ROS (detected by DCFH-DA, Supplementary Fig. 6e), hydrogen peroxide (Supplementary Fig. 6f) and aggravated the expression of phenotypic markers (Supplementary Fig. 6g).