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- W3097866009 endingPage "2850" @default.
- W3097866009 startingPage "2835" @default.
- W3097866009 abstract "Abstract Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by synovitis and the presence of serum autoantibodies. In addition, skeletal muscle weakness is a common comorbidity that contributes to inability to work and reduced quality of life. Loss in muscle mass cannot alone account for the muscle weakness induced by RA, but instead intramuscular dysfunction appears as a critical factor underlying the decreased force generating capacity for patients afflicted by arthritis. Oxidative stress and associated oxidative post-translational modifications have been shown to contribute to RA-induced muscle weakness in animal models of arthritis and patients with RA. However, it is still unclear how and which sources of reactive oxygen and nitrogen species (ROS/RNS) that are involved in the oxidative stress that drives the progression toward decreased muscle function in RA. Nevertheless, mitochondria, NADPH oxidases (NOX), nitric oxide synthases (NOS) and phospholipases (PLA) have all been associated with increased ROS/RNS production in RA-induced muscle weakness. In this review, we aim to cover potential ROS sources and underlying mechanisms of oxidative stress and loss of force production in RA. We also addressed the use of antioxidants and exercise as potential tools to counteract oxidative stress and skeletal muscle weakness." @default.
- W3097866009 created "2020-11-09" @default.
- W3097866009 creator A5004552128 @default.
- W3097866009 creator A5038537456 @default.
- W3097866009 creator A5081201379 @default.
- W3097866009 date "2020-11-01" @default.
- W3097866009 modified "2023-10-17" @default.
- W3097866009 title "Skeletal muscle redox signaling in rheumatoid arthritis" @default.
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