Elsevier

EBioMedicine

Volume 23, September 2017, Pages 12-19
EBioMedicine

Review
Muscle Weakness in Rheumatoid Arthritis: The Role of Ca2 + and Free Radical Signaling

https://doi.org/10.1016/j.ebiom.2017.07.023Get rights and content
Under a Creative Commons license
open access

Highlights

  • Muscle weakness is commonly reported by patients with rheumatoid arthritis (RA).

  • Intrinsic muscle weakness is important in the underlying mechanisms of muscle weakness associated with rheumatoid arthritis.

  • Enhanced Ca2 + release and peroxynitrite-induced stress contributes to RA-induced muscle weakness.

Abstract

In addition to the primary symptoms arising from inflammatory processes in the joints, muscle weakness is commonly reported by patients with rheumatoid arthritis (RA). Muscle weakness not only reduces the quality of life for the affected patients, but also dramatically increases the burden on society since patients' work ability decreases. A 25–70% reduction in muscular strength has been observed in pateints with RA when compared with age-matched healthy controls. The reduction in muscle strength is often larger than what could be explained by the reduction in muscle size in patients with RA, which indicates that intracellular (intrinsic) muscle dysfunction plays an important role in the underlying mechanism of muscle weakness associated with RA. In this review, we highlight the present understanding of RA-associated muscle weakness with special focus on how enhanced Ca2 + release from the ryanodine receptor and free radicals (reactive oxygen/nitrogen species) contributes to muscle weakness, and recent developments of novel therapeutic interventions.

Keywords

Rheumatoid arthritis
Muscle weakness
Ca2 +
 Ryanodine receptor
Nitrosative stress
Peroxynitrite

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