Endothelial progenitor cell dysfunction is a promising but not yet fully validated biomarker for stratifying cardiovascular risk in different phenotypes of obesity.
May aid CV risk stratification across obese phenotypes; leaves open whether EPC dysfunction predicts progression or events in prospective studies.
Obesity is common endocrine disorders that is characterized an increased prevalence worldwide for last decades. Based on the Adult Treatment Panel-III criteria subjects with established obesity and co-existing other metabolic abnormalities including dyslipidemia, insulin resistance (IR), increased fasting glucose and impaired glucose tolerance, are referred metabolically non-healthy, whereas obese individuals without these abnormalities might be defined as metabolically healthy. However, the risk stratification in both obesity phenotype patients is not accurately determined. Formerly endothelial progenitor cells (EPCs) were found a player in target organ damage at the different stages of obese. Probably, EPCs' dysfunction defined as lowered number and / or weak function of EPCs as a biomarker of altered endothelial function might be a predictor of cardiovascular (CV) risk in obese patients The aim of the short commentary is to summarize our knowledge regarding the role of endothelial progenitor cell dysfunction in prognostication of CV events in patients with established obesity.
No takes yet. Share an insight, caveat, or question.
A 2016 study studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: