Similarly, miR-216a was shown to be involved in EC aging, in atherosclerosis-related endothelial dysfunction by impairing the autophagy response to the accumulation of oxidized low-density lipoproteins36, and in macrophage pro-inflammatory M1 polarization by boosting the NF-κB pathway37,38. This evidence concerns the gene NFKB1 and endothelial dysfunction.