Although early neovascularization induced by SDF1α-eMSCs could provide an indirect beneficial effect on skeletal muscles, our in vitro experiments further revealed that the paracrine factors secreted by SDF1α-eMSCs protected myoblasts and promoted their migration under cellular starvation conditions simulating ischemia through the ERK and Akt pathways within the SDF1α/CXCR4 axis. This evidence concerns the gene CXCL12 and ischemia.