Balogh E, et al. - Researchers evaluated the impact of oxidative stress on cellular energy metabolism and pro-angiogenic/pro-inflammatory mechanisms of primary rheumatoid arthritis synovial fibroblast cells (RASFC) and human umbilical vein endothelial cells (HUVE). Metabolism was seen to be promoted in favour of glycolysis by oxidative stress, an impact that could contribute to the acceleration of inflammatory mechanisms and subsequent dysfunctional angiogenesis in RA. As per data, in patients with RA significant reduction in synovial tissue (ST) vascularity and angiopoietin 2 (Ang2)/tyrosine kinase receptor (Tie2) expression was demonstrated before and after administration of tumour necrosis factor inhibitors (TNFi).