Abstract
Diabetes mellitus (DM) is considered a leading cause of premature cardiovascular (CV) mortality and morbidity in general population and in individuals with known CV disease. Recent animal and clinical studies have shown that reduced number and weak function of endothelial progenitor cells (EPCs) may not only indicate to higher CV risk, but contribute to the impaired heart and vessels reparation in patients with DM. Moreover, EPCs having a protective impact on the vasculature may mediate the functioning of other organs and systems. EPCs dysfunction is probably promising target for DM treatment strategy, while the role of restoring of EPCs number and functionality in CV risk diminish and reduce of DM-related complications is not fully clear. The aim of the short commentary: to elucidate the causative role of EPCs dysfunction in DM patients.
Highlights
Diabetes mellitus (DM) is considered a leading cause of premature cardiovascular (CV) mortality and morbidity in general population and in individuals with known CV disease
Diabetes mellitus (DM) is a worldwide epidemic metabolic disease associated with increased cardiovascular (CV) complications, premature CV death, and a higher incidence of disability leading to social and economic burden [1]
DM was found as the important cause of atherosclerosis, coronary artery disease, chronic renal disease, and heart failure [2,3,4,5]
Summary
Diabetes mellitus (DM) is considered a leading cause of premature cardiovascular (CV) mortality and morbidity in general population and in individuals with known CV disease. The key role in the endothelial repair, vasculogenesis, neovascularization and attenuation of vasculature function plays endothelial progenitor cells (EPCs) derived from bone marrow and peripheral blood [14].
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