Abstract
Rheumatoid arthritis (RA) remains a desolating and devastating disease with a strong social impact on the world. Current drugs and therapies are showing poor responses toward RA due to its unknown progression. Evidence has shown that Extra Domain A fibronectin, recognized as a damage-associated molecular pattern (DAMPs), interacts with pathogen recognition receptors (PRR), which play a vital role in the erosion and degradation of joints. The post-translational modification and citrullination of fibronectin enhance the expression of EDA fibronectin (EDA+Fn). Fibronectin and its interacting receptors, such as TLR-4 may be a potential target for the treatment of RA. This review critically summarizes the recent discoveries and breakthroughs in the role of fibronectin and its isoforms in the pathogenesis and progression of RA.
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