Visfatin: An emerging adipocytokine bridging the gap in the evolution of cardiovascular diseases

Dakroub, Ali; Nasser, Suzanne A.; Kobeissy, Firas; Yassine, Hadi M.; Orekhov, Alexander; Sharifi‐Rad, Javad; Iratni, Rabah; El‐Yazbi, Ahmed F.; Eid, Ali H.

Abstract

Visfatin/nicotinamide phosphoribosyltransferase (NAMPT) is an adipokine expressed predominately in visceral fat tissues. High circulating levels of visfatin/NAMPT have been implicated in vascular remodeling, vascular inflammation, and atherosclerosis, all of which pose increased risks of cardiovascular events. In this context, increased levels of visfatin have been correlated with several upregulated pro-inflammatory mediators, such as IL-1, IL-1Ra, IL-6, IL-8, and TNF-α. Furthermore, visfatin is associated with leukocyte recruitment by endothelial cells and the production of adhesion molecules such as vascular cell adhesion molecule 1, intercellular cell adhesion molecule 1, and E-selectin, which are well known to mediate the progression of atherosclerosis. Moreover, diverse angiogenic factors have been found to mediate visfatin-induced angiogenesis. These include matrix metalloproteinases, vascular endothelial growth factor, monocyte chemoattractant protein 1, and fibroblast growth factor 2. This review aims to provide a comprehensive overview of the pro-inflammatory and angiogenic actions of visfatin, with a focus on the pertinent signaling pathways whose dysregulation contributes to the pathogenesis of atherosclerosis. Most importantly, some hypotheses regarding the integration of the aforementioned factors with the plausible atherogenic effect of visfatin are put forth for consideration in future studies. The pharmacotherapeutic potential of modulating visfatin's roles could be important in the management of cardiovascular disease, which continues to be the leading cause of death worldwide.

Citation

Dakroub, A., Nasser, S. A., Kobeissy, F., Yassine, H. M., Orekhov, A., Sharifi‐Rad, J., …Eid, A. H. (2021). Visfatin: An emerging adipocytokine bridging the gap in the evolution of cardiovascular diseases. Journal of Cellular Physiology, 236(9), 6282-6296. https://doi.org/10.1002/jcp.30345

• Journal Article Type: Article
• Acceptance Date: Feb 12, 2021
• Online Publication Date: Feb 26, 2021
• Publication Date: 2021-09
• Deposit Date: Jun 2, 2023
• Journal: Journal of Cellular Physiology
• Print ISSN: 0021-9541
• Electronic ISSN: 1097-4652
• Publisher: Wiley
• Peer Reviewed: Peer Reviewed
• Volume: 236
• Issue: 9
• Pages: 6282-6296
• DOI: https://doi.org/10.1002/jcp.30345
• Keywords: Cell Biology; Clinical Biochemistry; Physiology
• Additional Information: Received: 2020-12-04; Accepted: 2021-02-12; Published: 2021-02-26