Volume 58, Issue 4, Pages 801-810 (April 2013) Non-alcoholic steatohepatitis: The role of oxidized low-density lipoproteins  Sofie M.A. Walenbergh, Ger H. Koek, Veerle Bieghs, Ronit Shiri-Sverdlov  Journal of Hepatology  Volume 58, Issue 4, Pages 801-810 (April 2013) DOI: 10.1016/j.jhep.2012.11.014 Copyright © 2012 European Association for the Study of the Liver Terms and Conditions

Fig. 1 Schematic diagram illustrating the metabolic crosstalk between liver, adipose tissue, gut, arteries and systemic inflammation. The development of NASH is dependent on underlying mechanisms related to the metabolic syndrome, such as disturbed intestinal permeability, gut microbiota, increased systemic inflammation, vascular abnormalities, and adipose tissue dysfunction as a result of increased macrophage infiltration and insulin resistance. In turn, NASH by itself can exacerbate inflammation in these metabolic tissues, retaining a positive feedback mechanism. Journal of Hepatology 2013 58, 801-810DOI: (10.1016/j.jhep.2012.11.014) Copyright © 2012 European Association for the Study of the Liver Terms and Conditions

Fig. 2 Schematic illustration showing the involvement of oxLDL in the macrophage inflammatory response. Lipid-laden foamy macrophages express higher levels of the scavenger receptors CD36 and SR-A and produce more pro-inflammatory cytokines. Through interplay with surrounding cells, these cytokines further amplify the inflammatory response. Blocking macrophage uptake of oxLDL leads to macrophages smaller in size, less CD36 and SR-A expression and reduced inflammation. Modified from [135], reprinted by permission from Elsevier. Journal of Hepatology 2013 58, 801-810DOI: (10.1016/j.jhep.2012.11.014) Copyright © 2012 European Association for the Study of the Liver Terms and Conditions