Itaconate, an endogenous metabolite of the tricarboxylic acid (TCA) cycle, is known to have immunomodulatory and antimicrobial properties, but its role in the pathogenesis of rheumatoid arthritis (RA) is unclear. New research has explored whether itaconate could have therapeutic effects in RA by affecting the aggressive phenotype of fibroblast-like synoviocytes (FLSs).

RA-FLSs are known to have a dysregulated metabolic profile, and inhibition of glycolysis can decrease the proliferation and migration of RA-FLSs and ameliorates experimental arthritis. Having shown previously that itaconate metabolically regulates T cell differentiation and attenuates the severity of a model of T cell-driven autoimmune disease, Tada et al. sought to determine the effects of itaconate on RA-FLSs and its potential as a treatment for RA.