Fig. 2

Direct and indirect effects of hypoxia and/or HIF on the different cell types contributing to RA pathogenesis. References relevant to the indicated phenomena are provided in the scheme. The colors of the molecules name indicate if the molecule has effect on: inflammation (yellow), oxidative stress (cyan), energy metabolism (blue), angiogenesis (magenta), destruction (green). ACADVL very long-chain acyl-CoA dehydrogenase; ACSL, long-chain fatty acid-CoA ligase; ANGPLT, angiopoietin-like; CCL20, chemokine (C-C motif) ligand 20; CO, mitochondrial cytochrome; CS, citrate synthase; DLST, oxoglutarate dehydrogenase complex component E2; ENO, enolase; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; GLUT, glucose transporter; GPI, glucose phosphate isomerase; HADHA, hydroxyacyl-CoA dehydrogenase/3-ketoacyl-CoA thiolase/enoyl-CoA hydratase; HIF, hypoxia-inducible factor; HMGB, high-mobility group protein B; Hxk, hexokinase; IL, interleukin; LDH, lactate dehydrogenase; MMP, matrix metalloproteinase; NOX, NADPH oxidase; PFKP phosphofructokinase; PGD, phosphogluconate dehydrogenase; PLGF, placental growth factor; ROS, reactive oxygen species; SDF, stromal cell-derived factor; TIMP, tissue inhibitor of metalloproteinase; TNF, tumor necrosis factor; VEGF, vascular endothelial growth factor