Recent several preclinical studies have shown that the inhibition of CCL2 through anti-CCL2 antibody or CCR2 depletion can attenuate adverse left ventricular remodeling in MI mice, and silencing CCR2 gene through siRNA reduces inflammatory monocytes/macrophages recruitment in ischemic areas and improves heart function in MI mice (181). This evidence concerns the gene CCL2 and myocardial infarction.