Our findings demonstrate that a relationship exists between the HMGA1 rs146052672 variant and AMI, suggesting that defects at the HMGA1 locus may play a pathogenetic role in AMI, in the absence of T2DM and other cardiovascular risk factors.
The combined adjusted odds ratio estimates revealed that the rs146052672 variant genotype had an overall statistically significant effect on increasing the risk of development of T2D.
Multiple logistic regression confirmed that the rs146052672 was significantly associated with AMI (OR=2.54; p=0.002), and this association was independent of classical cardiovascular risk factors such as gender, hypertension, obesity and T2DM (for all, p<0.05).
Multiple logistic regression confirmed that the rs146052672 was significantly associated with AMI (OR=2.54; p=0.002), and this association was independent of classical cardiovascular risk factors such as gender, hypertension, obesity and T2DM (for all, p<0.05).
Our findings demonstrate that a relationship exists between the HMGA1 rs146052672 variant and AMI, suggesting that defects at the HMGA1 locus may play a pathogenetic role in AMI, in the absence of T2DM and other cardiovascular risk factors.
From a mechanistic point of view, our findings indicated that, by adversely affecting HMGA1 protein expression and function, the HMGA1 rs139876191 variant played a key role in this protective mechanism by downregulating the expression of vascular endothelial growth factor A (VEGFA), a major activator of neovascularization in DR.
Overall, our results indicate that the rs146052672</span> variant represents an early predictive marker of MetS, as well as a predictive tool for therapy.