Abstract
Advances in the field of vascular biology lead to the identification of endothelial progenitor cells (EPC) and to the development of EPC-based cell therapy to induce new vessel formation in ischemic tissues and to accelerate re-endothelialisation of injured vessels in human and various animals models. However, recent studies have shown that age and other risk factors for cardiovascular diseases, such as diabetes, reduce the availability of EPC and impair their function to varying degrees, leading to reduction in postischemic vessel growth. This review focus on the cellular and molecular mechanisms governing EPC-related functions and analyzes the impact of diabetes in this setting.
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