Dysfunction of Endothelial Cell Precursors in Heart Failure Development
Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2017, Vol 1, Issue 3
Abstract
Heart failure (HF) a leading cause of premature death in patients with established cardiovascular (CV) disease. Although the global burden of HF is increasing, there is no evidence regarding promising results that improves long-term clinical outcomes especially for HF with preserved and mid-regional pump function. In this context, determination of the vulnerable populations at higher risk of HF development and progression is very promising. Endothelial dysfunction (ED) plays a central role in the manifestation of HF regardless its phenotypes. There is a large body of evidence regarding that the endothelial progenitor cells (EPCs) as a component of endogenous vascular repair system could be modified by several stimuli including epigenetic factors and thereby they are involved in the pathogenesis of ED. However, there is unclear whether EPC dysfunction is only whiteness of HF or it could be a factor of HF manifestation in vulnerable population. The short communication is depicted the uncertain role of EPC dysfunction in pathogenesis of HF.Heart failure (HF) remainsa leading cause of mortality in patients with established cardiovascular (CV) disease [1,2]. Currently there is a strong trend toward reducing death rate due to HF associated with steady increased frequencies of newly manifested HF in developed countries, although in developing countries the HF mortality rate appears to be exaggeratedly high [3]. Identification of the vulnerable populations at higher risk of HF development and progression is now based on the early diagnosis of CV disease (atherosclerosis, hypertension, coronary heart disease, peripheral artery disease, and vasculitis) and metabolic states including diabetes, abdominal obesity, thyroid dysfunction, as well as other CV risk factors which may pre-exist CV diseases and particularly HF [4]. Endothelial dysfunction (ED) is considered an integral state in the development of HF regardless its phenotypes [5] and even contributes in clinical outcomes across all stages of CV continuum [6]. There is a large body of evidence regarding that the exhausted reparative ability of vasculature in resulting in several factors including pre-existing co-morbidities, some severe diseases that had appeared prior HF manifestation (trauma, infections, inflammatory diseases), and CV risk factors could be primary reasons for loss of endothelial cell integrity and shaping ED [7-9]. In this context, endothelial progenitor cells (EPCs) that are mobbed from bone marrow precursors and peripheral tissue residences and involved in reparative processes through differentiation and turn-into mature endothelial cells are promising biomarkers of ED with possible predictive value [10,11].
Authors and Affiliations
Alexander E Berezin
Keywords
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- EP ID EP572665
- DOI 10.26717/BJSTR.2017.01.000310
- Views 200
- Downloads 0
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