Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Endothelial dysfunction is thought to play a major role in the development and clinical complications of heart failure. Endothelial progenitor cells (EPCs) have been shown to provide an endogenous repair mechanism to counteract detrimental risk factor-induced effects and replace dysfunctional endothelium. The number and in vitro function of EPCs is altered in patients with heart failure, as a result of its pathophysiological mechanisms. EPCs could represent a substitutional marker to guide preventive or therapeutic interventions in this disease. Enhancing the number and functional capacity of EPCs with targeted interventions may elicit functional improvement in individuals with heart failure. However, the exact role of EPCs in heart failure and their potential therapeutic implications still remain to be elucidated.

Original publication

DOI

10.1016/j.atherosclerosis.2006.06.021

Type

Journal article

Journal

Atherosclerosis

Publication Date

12/2006

Volume

189

Pages

247 - 254

Keywords

Animals, Cells, Cultured, Endothelium, Vascular, Heart Failure, Humans, Neovascularization, Pathologic, Risk Factors, Stem Cells, Vascular Resistance