Our present study revealed that (1) OSM treatment preserved cardiac function and attenuated myocardial apoptosis and fibrosis in a mouse MI model; (2) OSM promoted angiogenesis in the infarct border zone after MI probably via upregulating angiogenic factors VEGF and bFGF; (3) the beneficial effect of OSM in MI mice was abrogated when OSM receptor Oβ was knocked out. This evidence concerns the gene FGF2 and myocardial infarction.