Oxidation in rheumatoid arthritis

摘要: Oxygen metabolism has an important role in the pathogenesis of rheumatoid arthritis. Reactive oxygen species (ROS) produced course cellular oxidative phosphorylation, and by activated phagocytic cells during bursts, exceed physiological buffering capacity result stress. The excessive production ROS can damage protein, lipids, nucleic acids, matrix components. They also serve as intracellular signaling molecules that amplify synovial inflammatory–proliferative response. Repetitive cycles hypoxia reoxygenation associated with changes perfusion are postulated to activate hypoxia-inducible factor-1α nuclear factor-κB, two key transcription factors regulated oxygenation cytokine stimulation, turn orchestrate expression a spectrum genes critical persistence synovitis. An understanding complex interactions involved these pathways might allow development novel therapeutic strategies for