Human adipose stromal cells (ASCs) secrete multiple angiogenic and antiapoptotic growth factors, making them a promising source for autologous cell therapy in cardiovascular disease. ASCs were isolated from subcutaneous fat and characterized by flow cytometry. They secreted vascular endothelial growth factor (VEGF), hepatocyte growth factor (HGF), and transforming growth factor-β (TGF-β) at levels that are bioactive. Hypoxia significantly increased VEGF secretion, and transfection with a VEGF plasmid further enhanced it. Conditioned media from hypoxic ASCs improved endothelial cell growth and reduced apoptosis. In a mouse model of hindlimb ischemia, ASCs significantly improved perfusion. These findings suggest that ASCs, which can be easily harvested and expanded, may be a novel therapeutic option for enhancing angiogenesis and cardiovascular protection. ASCs also have the potential to respond to hypoxia, which may regulate their growth factor secretion in response to ischemia. The study highlights the therapeutic potential of ASCs, both for their ability to secrete growth factors and for their pluripotency, which may allow them to differentiate into vascular cells. Future studies should explore whether ASCs can be directed toward cardiovascular differentiation to complement their growth factor secretion. The therapeutic potential of native or transduced ASCs for neovascularization and cardiovascular protection needs to be tested in controlled clinical trials.Human adipose stromal cells (ASCs) secrete multiple angiogenic and antiapoptotic growth factors, making them a promising source for autologous cell therapy in cardiovascular disease. ASCs were isolated from subcutaneous fat and characterized by flow cytometry. They secreted vascular endothelial growth factor (VEGF), hepatocyte growth factor (HGF), and transforming growth factor-β (TGF-β) at levels that are bioactive. Hypoxia significantly increased VEGF secretion, and transfection with a VEGF plasmid further enhanced it. Conditioned media from hypoxic ASCs improved endothelial cell growth and reduced apoptosis. In a mouse model of hindlimb ischemia, ASCs significantly improved perfusion. These findings suggest that ASCs, which can be easily harvested and expanded, may be a novel therapeutic option for enhancing angiogenesis and cardiovascular protection. ASCs also have the potential to respond to hypoxia, which may regulate their growth factor secretion in response to ischemia. The study highlights the therapeutic potential of ASCs, both for their ability to secrete growth factors and for their pluripotency, which may allow them to differentiate into vascular cells. Future studies should explore whether ASCs can be directed toward cardiovascular differentiation to complement their growth factor secretion. The therapeutic potential of native or transduced ASCs for neovascularization and cardiovascular protection needs to be tested in controlled clinical trials.