HMGB1 and atherosclerosis: Taken together, our findings provided evidence that the upregulation of miR-200a repressed the activation of the STAT3/HMGB1 axis by inhibiting EZH2 expression, thus suppressing cell injury, apoptosis, and inflammation while promoting viability of ox-LDL-induced HUVECs, which helped alleviate atherosclerosis progression.