Authors: ShengZhong Duan
Publish Date: 2014/08/08
Volume: 57, Issue: 8, Pages: 809-817
Abstract
Vascular remodeling is a pathological condition with structural changes of blood vessels Both insideout and outsidein hypothesis have been put forward to describe mechanisms of vascular remodeling An integrated model of these two hypotheses emphasizes the importance of immune cells such as monocytes/macrophages T cells and dendritic cells These immune cells are at the center stage to orchestrate cellular proliferation migration and interactions of themselves and other vascular cells including endothelial cells ECs vascular smooth muscle cells VSMCs and fibroblasts These changes on vascular wall lead to inflammation and oxidative stress that are largely responsible for vascular remodeling Mineralocorticoid receptor MR is a classic nuclear receptor MR agonist promotes inflammation and oxidative stress and therefore exacerbates vascular remodeling Conversely MR antagonists have the opposite effects MR has direct roles on vascular cells through nongenomic or genomic actions to modulate inflammation and oxidative stress Recent studies using genetic mouse models have revealed that MR in myeloid cells VSMCs and ECs all contribute to vascular remodeling In conclusion data in the past years have demonstrated that MR is a critical control point in modulating vascular remodeling Studies will continue to provide evidence with more detailed mechanisms to support this notionThis article is published under an open access license Please check the Copyright Information section for details of this license and what reuse is permitted If your intended use exceeds what is permitted by the license or if you are unable to locate the licence and reuse information please contact the Rights and Permissions team
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