Regarding these findings, our results suggest a compensatory increase in miR125a in response to I/R and endothelial dysfunction, but there is no evidence of the effectiveness of elevated miR125a to reduce levels of ICAM-1 and VCAM-1, and instead of miR-125a being a modulator of inflammation, it might be that inflammation upregulates miR-125a. This evidence concerns the gene VCAM1 and endothelial dysfunction.