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miR-216a is over-expressed in CAD patients. miR-216a attaches to 3' UTR of Smad3 and decreases its levels. Down-regulation of Smad3 leads to reduction of IκBα releasing NF-κB and enhancing its nuclear transport. Subsequent up-regulation of ICAM1 and VCAM1 enhances attachment of monocytes to endothelial cells promoting development of CAD (16).
