Successful tumour necrosis factor (TNF) blocking therapy suppresses oxidative stress and hypoxia-induced mitochondrial mutagenesis in inflammatory arthritis

• Main Authors: Biniecka, M, Kennedy, A, Ng, C.T, Chang, T.C, Balogh, E, Fox, E, Veale, D.J, Fearon, U, O'Sullivan, J.N
• Other Authors: DUKE-NUS MEDICAL SCHOOL
• Format: Article
• Published: 2020
• Subjects: mitochondrial DNA; oxygen; tumor necrosis factor inhibitor; vasculotropin; biological product; tumor necrosis factor alpha; arthritis; article; clinical article; clinical assessment; controlled study; human; immunohistochemistry; inflammation; lipid peroxidation; mitochondrial genome; mutagenesis; nucleotide sequence; oxidative stress; oxygen tension; synovitis; synovium; tissue oxygenation; visual analog scale; cell hypoxia; drug antagonism; drug effect; genetics; mitochondrion; mutation; reverse transcription polymerase chain reaction; rheumatoid arthritis; Arthritis, Rheumatoid; Biological Agents; Cell Hypoxia; DNA, Mitochondrial; Humans; Immunohistochemistry; Mitochondria; Mutagenesis; Mutation; Oxidative Stress; Oxygen; Reverse Transcriptase Polymerase Chain Reaction; Synovial Membrane; Tumor Necrosis Factor-alpha
• Online Access: https://scholarbank.nus.edu.sg/handle/10635/181630
• Institution: National University of Singapore

10.1186/ar3424