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. 2012 Sep 3;2012:570598. doi: 10.1155/2012/570598

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Copyright © 2012 Ana Paula Villela Dantas et al.

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Hypothesis for detrimental estrogen responses in the diabetic vasculature: Type 2 diabetes mellitus-(T2DM-) related changes in the vessel wall include decrease of nitric oxide (NO) and concomitant increase of reactive oxygen species (ROS) and endothelin-1 (ET-1) production; as well as increased activation of signaling pathways of Nuclear Factor-κB (NF-κB); mitogen-activated protein kinases (MAPK) and receptors for advanced glycation products (RAGE). In a healthy vasculature (a), with favorable balance of estrogen receptors (ER), estrogen beneficially acts to modulate these factors and to maintain homeostasis. Nevertheless, T2DM adversely modify the balance in expression and/or activity of ERs in a manner that the effects of estrogen are negatively modulated to enhance the existing damage in vascular function (b).