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. 2018 Feb 13;8:2952. doi: 10.1038/s41598-018-21087-5

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Hypothetical scheme of putative signaling mechanisms induced by aldosterone/MR over-activation in obesity. On one hand, aldosterone/MR induces ROCK activity through decreased PKG-1a, resulting in vascular hypercontractility of arteries from obese db/db mice. In obesity-related diabetes, ROCK may also contribute to vascular insulin resistance independently of MR. In addition, vascular remodeling, due to increased pro-fibrotic and pro-inflammatory signaling, is also regulated, in part, by MR. MLC: myosin light chain; Mypt1: myosin light chain phosphatase subunit 1; MR: mineralocorticoid receptor; PKG-1α: cGMP-dependent protein kinase G type 1 isoform alpha; ROCK: Rho kinase; p: phosphorylated.