Nitrosative modifications of the Ca2+ release complex and actin underlie arthritis-induced muscle weakness.

Objective Skeletal muscle weakness is a prominent clinical feature in patients with rheumatoid arthritis (RA), but the underlying mechanism(s) is unknown. Here we investigate the mechanisms behind arthritis-induced skeletal muscle weakness with special focus on the role of nitrosative stress on intracellular Ca 2+ handling and specific force production.