AGT and cardiac hypertrophy: Previous studies have found that CaMKIIδinhibitors alleviate myocardial cell hypertrophy induced by angiotensinII, phenylephrine, and electric field stimulation, while overexpression of CaMKIIδB or CaMKIIδC enhances myocardial cell hypertrophy [25,26];ASF binds to protein phosphatase1γ (PP1γ), which can increase alternative splicing of CaMKIIδ and promote the expression of CaMKIIδB/C mRNA variants [27]; Overexpression of myocardial PP1γ enhances CaMKIIδ activity and reduces myocardial hypertrophy [28].