In conclusion, these data are consistent with a novel role for 11β-HSD1 in the regulation of acute inflammation following MI, via suppression of CXCL2 and CXCl5 chemoattractant expression and are supportive of cardiac fibroblasts as a key site for glucocorticoid regeneration by 11β-HSD1 following myocardial injury. This evidence concerns the gene CXCL2 and myocardial infarction.