DDAH1 and endothelial dysfunction: In the present study, we provided evidence that DMY attenuated TNF-α-induced endothelial dysfunction through downregulation of miR-21 expression, resulting in an increased expression and activity of DDAH1, which in turn leads to decreasing both intracellular and extracellular ADMA levels and enhancing eNOS (ser1177) phosphorylation and NO production.