It is well established that ROS contributes to hypertension by impairing vasodilation, increasing vascular resistance and cellular proliferation, activating matrix metalloproteinases (MMPs), and promoting extracellular matrix protein deposition, etc. [72,73] Notably, the knockdown of GW182 did not affect this translation process, suggesting that the translational regulatory mechanism of Ago2 in mitochondria may be different from that in the cytoplasm.[8]. Here, AGO2 is linked to hypertensive disorder.