Furthermore, we discover that miR-30 regulates exogenous FAO in cultured ECs, promoting oxidative stress, lipid peroxidation and endothelial dysfunction (i.e., reduced eNOS expression) and that inhibition of the miR-30 family in vivo reduces markers of oxidative stress and DNA damage/senescence in the coronary microvasculature of db/db mice. Here, NOS3 is linked to endothelial dysfunction.