AGTR2 and cardiac hypertrophy: It is conceivable that cardiac hypertrophy, capillary rarefaction, and a female-specific loss of cardio-reparative Agtr2 in the setting of a very high expression of pro-hypertrophic miR-208a could have contributed to increased myocardial structural damage in the form of cardiomyocyte loss and scarring as shown in Fig. 8f.