Why the study?
Does hypercholesterolemia decrease the count and function of circulating EPCs in postmenopausal females?
Does hypercholesterolemia decrease the count and function of circulating EPCs in postmenopausal females?
Hypercholesterolemia in postmenopausal women is associated with decreased endothelial progenitor cell count and function, linked to reduced nitric oxide production, highlighting a potential mechanism for increased cardiovascular risk.
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Hypercholesterolemia was associated with EPC dysfunction in postmenopausal women; leaves open causal role in CV risk and need for prospective studies.
Endothelial progenitor cells (EPCs) contribute to the endogenous endothelial repair program during hypercholesterolemia. EPC count and migratory and proliferative capacities remain unchanged in the premenopausal female with hypercholesterolemia. However, the changes of count and activity of circulating EPCs in the hypercholesterolemic postmenopausal females are unknown. Here, we find that the migratory and proliferative capacities of circulating EPCs were decreased in patients with hypercholesterolemia versus normocholesterolemia. No significant differences were found between postmenopausal females and age-matched males. NO production showed positive correlation with the activity and count of circulating EPCs in patients with hypercholesterolemia. Flow-mediated dilatation (FMD) is directly interrelated with EPC counts and function. Our findings reveal that decreased EPC count and endothelial dysfunction lead to less NO production in hypercholesterolemic postmenopausal females. Maintaining the EPC numbers and activity might be emerging as a potential therapeutic strategy to reduce the risk of cardiovascular injury in elder women.
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Luo et al. (2018) studied this question.
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