Endothelial progenitor cells (EPCs) are a special type of stem cells, derived from bone marrow that can be mobilized to the peripheral circulation in response to many stimuli. EPCs play a crucial role in the vascular repair, as well as in neovascularization processes. Recent studies have shown that EPCs are impaired, both in number and function, in diabetic patients independently of other cardiovascular risk factors.
Accelerated atherosclerosis is probably the most devastating among diabetes complications and endothelial dysfunction might be the beginning of the atherosclerosis. The impairment of EPCs seems to significantly contribute to atherogenesis and atherosclerotic disease progression in diabetes.
Autologous EPCs therapy is a promising treatment option for vascular complications requiring therapeutic revascularization and vascular repair. Diabetic patients represent a population that may benefit from cell-based therapy; however, the dysfunction of their endogenous cells may limit the feasibility of this approach. In fact, EPCs isolated from these patients for autologous cell transplantation may retain their dysfunctional characteristics in vivo and as a consequence display a reduced capacity to improve therapeutic neovascularization.
In the present review, we summarize the most relevant mechanisms underlying EPC dysfunction in diabetes.