AGT and persistent truncus arteriosus: We showed here that the phosphorylated p38 (p-p38) level was significantly increased in the myocardium of TAC mice and in Ang II-stimulated H9C2 cardiomyocytes, while SYT1 KO or silencing exacerbated these effects, suggesting that SYT1 can adversely regulate cardiac hypertrophy mainly via affecting the phosphorylation of p38.