It is upregulated by hypoxia in a hypoxia-inducible factor 1 (HIF-1α)-dependent manner, and facilitates chemotaxis, stem-cell recruitment and cardiomyocyte survival via its G-protein coupled receptor, CXCR47 SDF-1α and CXCR4 are up-regulated in the heart in both experimental and clinical studies of MI.8 This evidence concerns the gene CXCR4 and myocardial infarction.