Mismatched effects of receptor interacting protein kinase-3 on hepatic steatosis and inflammation in non-alcoholic fatty liver disease

Figure 6 Conceptual diagram. GSK'843 treatment decreases neutrophil recruitment markers, including CXCL1 and CXCL2, thereby reducing neutrophil recruitment to the tissue. However, RIP3 inhibition increases de novo fat synthesis while decreasing VLDL secretion. RIP3: Receptor interacting protein kinase-3; CXCL1: Chemokine (C-X-C motif) ligand-1; CXCL2: Chemokine (C-X-C motif) ligand-2; VLDL: Very-low-density lipoproteins.