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. 2019 Jan 17;9:1857. doi: 10.3389/fphys.2018.01857

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Copyright © 2019 Teodoro, Nunes, Rolo, Reis and Palmeira.

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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Schematic diagram representing the central role of oxidative stress and inflammation, guided by insulin resistance, hyperglycemia and hyperlipidemia (gluco and lipo toxicity), in the vascular changes underlying the progression of micro and macrovascular complications of diabetes. AGEs, advanced glycation end products; CRP, C-reactive-protein; EC, endothelial cells; eNOS, endothelial nitric oxide synthase; ICAM-1, intracellular adhesion molecule-1; IL, interleukin; IFN, interferon; JNK, c-jun NH2-terminal kinase; LDL, Low Density Lipoprotein; MCP-1 (CCL-2), Monocyte chemotactic protein-1; NF-κB, nuclear factor-κB; NO, nitric oxide; PKC, protein kinase C; RAGEs, receptor for AGEs; ROS, reactive oxygen species; TLR, Toll-Like Receptor; TNF-α, tumor necrosis factor-alfa; VSMC, vascular smooth muscle cells; VCAM-1, vascular cell adhesion molecule; vWF, von Willebrand factor.