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. 2019 Aug 23;10:584. doi: 10.3389/fendo.2019.00584

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Copyright © 2019 Gorini, Kim, Infante, Mammi, La Vignera, Fabbri, Jaffe and Caprio.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Aging is associated with vascular damage characterized by inflammation, vascular thickening, arterial stiffness and overproduction of reactive oxygen species (ROS). In this setting, mineralocorticoid receptor (MR) activation in endothelial cells can contribute to amplify cardiovascular adverse outcomes, exacerbating vascular stiffness through the induction of augmented ROS production, vascular inflammation and collagen deposition, finally leading to endothelial dysfunction and atherosclerosis. eNOS, endothelial nitric oxide synthase; NOX4, NADPH Oxidase 4; ICAM1, Intercellular Adhesion Molecule 1; VCAM1, vascular cell adhesion molecule 1.