Our results showed that miR-206 inhibitor alleviated ischemia-reperfusion-induced arrhythmias, indicated by the lower extent of changes in heart rate (HR), PR interval, rate pressure product (RPP), and mean arterial pressure (MAP). miR-206 inhibitor also downregulated the serum creatine kinase isoenzyme (CKMB) and cardiac troponin I (cTnI) levels in mice under myocardial ischemia-reperfusion (IR) process.
It is therefore proposed that repression of the phosphoinositide 3-kinase/Akt/endothelial nitric oxide synthase signal transduction pathway by miR-206 downregulates angiogenesis contributing to the pathophysiology of coronary artery disease.