EPC Dysfunction and Immune Networks: Translating Opportunities for 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. Recent studies emphasize the relevance of the endothelial homeostasis in the control of CV risk, but the clinical relevance of these findings is starting to be appreciated. 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. In the present narrative review, we aimed to compile and critically appraise all the current evidence linking inflammation and immune pathways with a compromised EPC functionality.

A mounting body of evidence points to an inflammation-driven traditional CV risk factorsrelated EPC dysfunction. The effect of aging on EPC was associated with the CXCR4 pathway, whereas that of hypertension was related to TNFα. Activation of Akt/eNOS was observed in response to diabetes- and dyslipidemia-related traits. Inflammation and oxidative stress underlie the EPC dysfunction during smoking.

Inflammatory and immune networks can be proposed as feasible biomarkers for risk stratification in personalized medicine schemes.