Visfatin: An emerging adipocytokine bridging the gap in the evolution of cardiovascular diseases. Issue 9 (26th February 2021)
- Record Type:
- Journal Article
- Title:
- Visfatin: An emerging adipocytokine bridging the gap in the evolution of cardiovascular diseases. Issue 9 (26th February 2021)
- Main Title:
- Visfatin: An emerging adipocytokine bridging the gap in the evolution of cardiovascular diseases
- Authors:
- 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:
- 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 modulatingAbstract: 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. Abstract : 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. 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. … (more)
- Is Part Of:
- Journal of cellular physiology. Volume 236:Issue 9(2021)
- Journal:
- Journal of cellular physiology
- Issue:
- Volume 236:Issue 9(2021)
- Issue Display:
- Volume 236, Issue 9 (2021)
- Year:
- 2021
- Volume:
- 236
- Issue:
- 9
- Issue Sort Value:
- 2021-0236-0009-0000
- Page Start:
- 6282
- Page End:
- 6296
- Publication Date:
- 2021-02-26
- Subjects:
- adipocytokine -- atherosclerosis -- cardiovascular disease -- inflammation -- NF‐κB -- visfatin
Physiology -- Periodicals
Cell physiology -- Periodicals
571.6 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1097-4652 ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1002/jcp.30345 ↗
- Languages:
- English
- ISSNs:
- 0021-9541
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 4955.020000
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 26704.xml