Bone marrow-derived MSCs from aged donors were shown to have worse proliferation and differentiation capacity28,30–33 and were less effective for tissue repair after ischemic injury; for example, in an animal model of myocardial infarction.33 In contrast to bone marrow-derived MSCs, the number of ADSCs in fat tissue, as evaluated by flow cytometry, does not decrease with age.34,35 However, their clonogenic and proliferation capacity declines36–40 as does the differentiation potential34,36,41 and the production of vascular endothelial growth factor (VEGF).42 This evidence concerns the gene VEGFA and myocardial infarction.