Abstract

Diabetes mellitus remains a leading factor contributing increased morbidity and mortality worldwide. The development and progression of DM associates with microvascular and macrovascular complications linked the DM with cardiovascular events. The impaired ability of endothelium to repair the injury and restore integrity depends in part on number and function of endothelial progenitor cells (EPCs). The mechanisms underlying EPC dysfunction in DM predominantly include weak bone marrow mobilization, decreased proliferation, and shortened survival. The weak function and lowered number of EPCs obtained from peripheral blood were recently found in 1 type and 2 type of DM. It has suggested that glucose toxicity, lipid toxicity, inflammation and oxidative stress may directly and indirectly via several molecular mechanisms worse of EPCs function and, however, lead to deficiency of circulating angiopoetic progenitors. Epigenetic changes are considered important key to understand whether EPCs dysfunction is reversible setting or not. The aim of editorial is to discuss around the role of epigenetic changes in EPCs in linking of DM with cardiovascular risk.