Fig. 8
![Fig. 8](http://media.springernature.com/full/springer-static/image/art%3A10.1186%2Fs13075-017-1478-7/MediaObjects/13075_2017_1478_Fig8_HTML.gif)
Proposed mechanism of the protective effects of PPARβ/δ activation in systemic lupus erythematosus (SLE) endothelial dysfunction. SLE plasma incubation induced endothelial dysfunction in human umbilical cord vein endothelial cells (HUVECs) by sequential activation of endoplasmic reticulum (ER)-stress and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. PPARβ/δ activation inhibited both ER stress and NADPH oxidase-driven reactive oxygen species (ROS) production reducing nitric oxide (NO) inactivation. AN, active nephritis