Fig. 2

Mechanisms of ROS-induced endothelial dysfunction in diabetic vascular complications. In the diabetic state, oxidative stress induced by hyperglycaemia, hyperlipidaemia, increased resistin and insulin resistance leads to physiological dysfunction of endothelial cells. It accelerates the occurrence and development of diabetic vascular complications through different mechanisms. Abbreviations: ROS, reactive oxygen species; APN,adiponectin; Nox, Nicotinamide adenine dinucleotide phosphate oxidase; ER, endoplasmic reticulum; MAPK, mitogen-activated protein kinase; PPARδ, peroxisome proliferator-activated receptor δ; PI3K, phosphatidylinositol 3 -kinase; Akt, protein kinase B; PKC, protein kinase C; NF-κB, nuclear factor kappa B; TNF-α, tumor necrosis factor α; IKK, inhibition of the NF-κB (IκB) kinase; Grb, Growth Factor Receptor-Bound Protein; SGLT2, Sodium-glucose Transporter2; DAG, diacylglycerol; FFA, free fatty acid; ERK1, Extracellular Signal Regulated Kinase 1; AGEs,advanced glycation end products; RAGE, receptor for AGEs; glyLDL, glycated low-density lipoproteins; ox-LDL, oxidized low-density lipoproteins; LOX-1, Lectin-like ox-LDL receptor-1; ET-1, Endothelin-1; EMPs, Endothelial microparticles; VCAM-1, Vascular cell adhesion molecule-1; VEGF, Vascular endothelial growth factor; VWF, Von Willebrand factor; eNOS, endothelial nitric oxide synthase; ICAM-1, Intercellular cell adhesion molecule-1. Figure was drawn by the authors using Adobe Illustrator tools