MiR-106 can downregulate the expression of MFN2, exacerbating cardiac hypertrophy induced by transverse aortic constriction (TAC) or angiotensin II (Ang II) pressure overload, which is associated with mitochondrial dysfunction, including mitochondrial cristae defects, the considerable depolarization of the mitochondrial membrane, and mtROS production, suggesting that high miR-106 expression levels promote mitochondrial dysfunction in cardiac hypertrophy (Guan et al., 2016). Here, AGT is linked to cardiac hypertrophy.