SMAD3 and coronary artery disorder: Our previous work showed that plasma miR-216a level increases in aged patients with coronary artery disease compared with healthy controls; experimental results further showed that stable expression of miR-216a can contribute to a premature senescence-like phenotype in human endothelial cells, inhibit endothelial proliferation, and activate inflammatory responses by inhibiting SMAD family member 3 (Smad3) expression [5].