"Obesity Paradox" in Heart Failure: The Possible Role of Progenitor Endothelial Cell Dysfunction
Alexander E Berezin*
Therapeutic Unit, Private Hospital “Vita-Center”, Zaporozhye, Ukraine
- *Corresponding Author:
- Alexander E Berezin
Therapeutic Unit, Private Hospital “Vita-Center”
E-mail: [email protected]; [email protected]
Received date: December 17, 2016; Accepted date: January 27, 2017; Published date: February 03, 2017
Citation: Berezin AE (2017) “Obesity Paradox” in Heart Failure: The Possible Role of Progenitor Endothelial Cell Dysfunction. Cell Dev Biol 6:179. doi:10.4172/2168-9296.1000179
Copyright: © 2017 Berezin AE. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
The “obesity paradox” phenomenon is referred to as a U-shaped curve between long-term prognosis and body mass index in heart failure patients. There is a large body of evidence regarding the regulatory role of visceral adipose tissue-related adipocytokines in activity of endogenous repair system. The reparation of myocardium and endothelium may strongly enhance by differentiation and mobbing of endothelial progenitor cells (EPCs). They improve angiogenesis and collateral vessel growth, as well as counteract vascular injury. It has suggested that several metabolic factors frequently associated with HF may increase the number of circulating EPCs, which mediate repair processes and collaborate with obese. In contrast, decreased number and/or weak functionality of EPCs relate with altered endogenous repair system and may negatively contribute in HF development. Finally, moving across recently received evidence “obesity paradox” could be elucidated as a result of interplaying of trigging repair systems and ability of EPCs to response on challenges enhancing reparative potency in target organs, i.e. myocardium, vascular wall and endothelium.