In 2018, Goldstone et al. observed that while SDF-1α exerted a proangiogenic effect after infarction, it did not change the proportion of circulating bone marrow-derived endothelial cells, suggesting that SDF-1α’s proangiogenic effect likely arises via formation of new blood vessels from pre-existing endothelial cells as opposed to bone marrow-associated vasculogenesis (de novo blood vessel formation)48. Here, CXCL12 is linked to infarction.