Fig. 1.

Central roles of miR-122 in HF, hypertension, MI, atherosclerosis and atrial fibrillation. MiR-122 has been shown to promote apoptosis, inflammation, fibrosis, pathological hypertrophy and remodeling in the cardiovascular system; decrease the LVEF, LVFS and cardiac contractility; and increase NT-proBNP and ROS generation, leading to arrhythmia and cardiovascular dysfunction. Therefore, miR-122 can cause cardiovascular fibrosis and heart dysfunction, ultimately resulting in hypertension, atherosclerosis, MI and HF. MI myocardial infarction, HF heart failure, ROS reactive oxygen species, LVFS left ventricular fractional shortening, LVEF left ventricular ejection fraction