EPC dysfunction and immune networks: translating opportunities for the clinical setting in personalized medicine.

Cardiovascular (CV) risk stratification is suboptimal if solely based on traditional CV risk factors, since individuals with similar risk profiles could exhibit diverging CV outcomes. Thus, there is a need for new risk factors to be identified and implemented. Recent studies emphasize the relevance of the endothelial homeostasis in the control of CV risk burden, but the clinical relevance of these findings is starting to be appreciated. However, gaining insight into the actual players involved in this phenomenon would lead to the identification of novel biomarkers. Due to their central role in vascular repair, Endothelial Progenitor Cells (EPC) are promising candidates for this issue. Since excessive inflammation or imbalanced immune responses are known to underlie numerical or functional alterations of EPC, it can be speculated that these mediators may be considered as biomarkers for risk stratification. Actually, a mounting body of evidence seems to point to an inflammation-driven traditional CV risk factors-related EPC dysfunction. Therefore, in the present review we summarized the evidence highlighting a link between inflammation and immune pathways with a compromised EPC functionality, aiming to identify feasible biomarkers for risk stratification in personalized medicine schemes.