The pro-fibrosis effects mediated by miR-223-3p were through targeting RAS p21 protein activator (RASA1), a RAS signal negative regulator, to upregulate the downstream MAPK and PI3K/AKT signaling pathways with increasing the phosphorylation of MAPK kinase 1/2 (MEK1/2), ERK1/2, and AKT, leading to myocardial fibrosis and deterioration of ventricular function (85). Here, AKT1 is linked to Myocardial fibrosis.