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dothelial progenitor cells (EPC) participate in angiogenesis and vascular homeostasis by incorporating into the endothelium of damaged vessels and, perhaps more importantly, exhibiting potent angiogenic paracrine effects (1). EPC are embedded in the microenvironment of bone marrow stromal and endothelial cells and translocate to the circulation upon NO-mediated signaling (2). Additional mobilizing pathways include extracellular signal-regulated kinases (ERK)/matrix metalloproteinase-9 (MMP-9)-mediated release of soluble c-Kit ligand (3). EPC participate in postnatal growth of new blood vessels and/or are home to sites of endothelial damage, maintaining endothelial integrity and function. Circulating EPC numbers are tightly correlated to endothelial function and serve as an independent predictor for cardiovascular diseases (4). Functional properties of EPC may be of equal or greater importance than quantitative alterations. A variety of functional limitations of progenitor cells from patients with coronary artery disease or diabetes, or from aged individuals, have been shown in the past (5–8). Identifying the mechanisms underlying EPC dysfunction in various diseases may lead to the development of treatments for dysfunctional EPC, as well as improved cardiovascular outcome in selected patient groups. This includes drug-mediated improvements of endogenous EPC number and function, as well as ex vivo treatment of autologous dysfunctional EPC before transplantation to ischemic sites after myocardial infarction. In this issue of Molecular Medicine, Humpert and colleagues (9) report on insulin’s beneficial effects on the clonogenic potential of EPCs derived from patients with type 2 diabetes (Figure 1). Diabetes is associated with an increased risk for cardiovascular disease, possibly due to impairment of the endogenous vascular repair capacity (6). Under physiological conditions, endothelial nitric oxide synthase (eNOS)

The IGF-1 Receptor as a Therapeutic Target to Improve Endothelial Progenitor Cell Function