The process of atherosclerosis is multifactorial and involves many mechanisms. The majority
of published works have identified endothelial dysfunction as the first step in a cascade of
events that culminates in plaque formation. Among the various mechanisms that occur following
the attack on the vessel wall, it is thought that stem cells in the form of endothelial
progenitor cells (EPCs) are the endothelial protection mechanism.
Factors identified as cardiovascular risk factors, or rather those conditions which suppose a
threat to the vessel wall, should therefore be associated with low levels of EPCs. To date
this link has been shown in hypertension, diabetes, hyperlipidaemia, and smoking.
Furthermore, the lack of wall protection in situations of low levels of EPCs is clearly a
biomarker of cardiovascular morbidity and mortality.
On the other hand, the correction of a risk factor allows recuperation of EPCs and is
therefore showing itself to be a promising tool for measuring therapeutic efficacy.
The tools for correcting EPC levels are not clearly defined. The effect of statins on levels
of EPC has been shown, and the low levels of EPCs in diabetes seem to be susceptible to
treatment with statins.
The role of glucagon-like peptide (GLP-1) is slowly being elucidated but the actual mechanism
of its potential endothelial protection is unknown, and its effect on EPCs has not been
Liraglutide, a long-acting GLP-1 analogue, could also be an interesting option for long-term
vessel wall protection, but to date its ability to correct cardiovascular biomarkers such as
EPCs has not been studied.