Interestingly, we found 7 novel functional loci (CBFA2T3, ZMIZ1, DIP2B, SCNN1D/ACAP3, TMEM105, CAMK2G, and MAPK1) that CAD-associated super enhancer SNPs were clustered into the same or neighboring super enhancers.
Moreover, the p38 MAPK signaling pathway might be involved in the pathogenesis of EMT induced by IL-33, which was consistent with the in vivo results of the kidney specimens from the control and CAD patients.
These data indicate that defects in SDF-1-triggered EPC-adhesion contribute to the functional impairment of EPCs in CAD, and that ERK-2 represents a new therapeutic target for functional improvement of EPC adhesion in CAD.
Polymorphism of IL-12 p40 gene was not found to be associated with the presence or severity of CAD, suggesting that it does not play an important role in the development of this disease.