C-Type of Natriuretic Peptide and Progenitor Endothelial Cell Dysfunction: The Link to Heart Failure Development

C-type of natriuretic peptide (CNP) is a promising biomarker of heart failure (HF) development and HFrelated clinical outcomes. Recent clinical studies have shown that elevated level of CNP strongly related to cardiac hemodynamic overload, myocardial ischemic injury, endothelial dysfunction, early atherosclerorsis, and worsening vascular repair. Whether CNP plays a regulatory role in restoring endothelium structure and function through modulating repair capacity of endothelial progenitor cells (EPCs) is not fully clear. However, CNP counteracts angiotensin II, which mediates NF-kappaB-dependent pro-inflammatory genes, peroxisome proliferator-activated receptor-α and –γ genes, NADPH/NADH oxidase genes in EPCs, deficiency of which is considered a marker of HF development and advance. The aim of the short comment is to discuss the role of CNP as mediator of vascular reparation and a marker of restoring of endothelial function in HF patients