Obesity is associated with increased cardiovascular morbidity and mortality in part due to vascular abnormalities such as endothelial dysfunction and arterial stiffening. The hypertension and other health complications that arise from these vascular defects increase the risk of heart diseases and stroke. Prooxidant and proinflammatory signaling pathways as well as adipocyte-derived factors have emerged as critical mediators of obesity-associated vascular abnormalities. Designing treatments aimed specifically at improving the vascular dysfunction caused by obesity may provide an effective therapeutic approach to prevent the cardiovascular sequelae associated with excessive adiposity. In this review, we discuss the recent evidence supporting the role of oxidative stress and cytokines and inflammatory signals within the vasculature as well as the impact of the surrounding perivascular adipose tissue (PVAT) on the regulation of vascular function and arterial stiffening in obesity. In particular, we focus on the highly plastic nature of the vasculature in response to altered oxidant and inflammatory signaling and highlight how weight management can be an effective therapeutic approach to reduce the oxidative stress and inflammatory signaling and improve vascular function.
Skip Nav Destination
Review Article| June 30 2017
Oxidative and inflammatory signals in obesity-associated vascular abnormalities
John J. Reho ;
1Department of Pharmacology, University of Iowa, Iowa City, Iowa, U.S.A.
2Fraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, Iowa, U.S.A.
3Obesity Research and Education Initiative, University of Iowa, Iowa City, Iowa, U.S.A.
4Center for Hypertension Research, University of Iowa, Iowa City, Iowa, U.S.A.
Correspondence: Kamal Rahmouni (email@example.com)
Search for other works by this author on:
- Views Icon Views
- Share Icon Share
John J. Reho, Kamal Rahmouni; Oxidative and inflammatory signals in obesity-associated vascular abnormalities. Clin Sci (Lond) 15 July 2017; 131 (14): 1689–1700. doi: https://doi.org/10.1042/CS20170219
Download citation file:
Don't already have an account? Register
Get Access To This Article
Buy This Article