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Crosstalk between adipose tissue and blood vessels in cardiometabolic syndrome: implication of steroid hormone receptors (MR/GR)

  • Sarah Elisabeth Louise Even , Maria Gabriela Dulak-Lis , Rhian M. Touyz and Aurelie Nguyen Dinh Cat EMAIL logo
Published/Copyright: September 4, 2014

Abstract

Crosstalk between adipose tissue and blood vessels is vital to vascular homeostasis and is disturbed in cardiovascular and metabolic diseases such as hypertension, diabetes and obesity. Cardiometabolic syndrome (CMS) refers to the clustering of obesity-related metabolic disorders such as insulin resistance, glucose and lipid profile alterations, hypertension and cardiovascular diseases. Mechanisms underlying these associations remain unclear. Adipose tissue associated with the vasculature [known as perivascular adipose tissue (PVAT)] has been shown to produce myriads of adipose tissue-derived substances called adipokines, including hormones, cytokines and reactive oxygen species (ROS), which actively participate in the regulation of vascular function and local inflammation by endocrine and/or paracrine mechanisms. As a result, the signaling from PVAT to the vasculature is emerging as a potential therapeutic target for obesity and diabetes-related vascular dysfunction. Accumulating evidence supports a shift in our understanding of the crucial role of elevated plasma levels of aldosterone in obesity, promoting insulin resistance and hypertension. In obesity, aldosterone/mineralocorticoid receptor (MR) signaling induces an abnormal secretion of adipokines, ROS production and systemic inflammation, which in turn contribute to impaired insulin signaling, reduced endothelial-mediated vasorelaxation, and associated cardiovascular abnormalities. Thus, aldosterone excess exerts detrimental metabolic and vascular effects that participate to the development of the CMS and its associated cardiovascular abnormalities. In this review, we focus on the physiopathological roles of corticosteroid receptors in the interplay between PVAT and the vasculature, which underlies their potential as key regulators of vascular function.


Corresponding author: Aurelie Nguyen Dinh Cat, PhD, BHF Glasgow, Cardiovascular Research Centre, University of Glasgow, 126 University Place, Glasgow, G12 8TA, UK, Phone: +44 141-330-8015, Fax: +44 141-330-3360, E-mail:

Acknowledgments

Work from the author’s laboratory was supported by grants from the Canadian Institutes of Health Research (CIHR) and grants from the British Heart Foundation (BHF). RMT is supported through a BHF Chair.

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Received: 2014-3-20
Accepted: 2014-8-6
Published Online: 2014-9-4
Published in Print: 2014-8-1

©2014 by De Gruyter

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