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A β toxicity was inhibited by insulin-like growth factor-I (IGF-I) and by overexpressing GRX1 or TRX1
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In RA, ROS are thought to directly contribute to destructive and proliferative synovitis and, thus, play an essential role in pathophysiology of RA.[3,4] Moreover, high levels of ROS can contribute to osteoclast differentiation via RANKL signaling, inducing bone and cartilage destruction
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