Consistent with these findings of impaired mobilisation of Lin-/VEGF-R2+ EPCs and SDF-1 downregulation are recent reports that SDF-1 is crucial in mobilizing progenitor cells[66] and that direct application of SDF-1 to rats with myocardial infarction reduced the infarction size, probably by stimulating migration of progenitor cells to the heart thereby altering postinfarction vascular remodeling[67]. This evidence concerns the gene CXCL12 and infarction.