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We treated hepatocytes with auranofin, which inhibits redox-active selenoproteins, including thioredoxin reductases and, at the dose used here, glutathione peroxidases 1, 2, 3, 4, and 6 (Chaudiere and Tappel, 1984, Roberts and Shaw, 1998, Scarbrough et al., 2012)

Excessive proliferation of FLSs and the release of pro-inflammatory factors are critical drivers of synovial inflammation in RA

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doi: 10.1002/pros.21158