Rheumatoid arthritis (RA) is a chronic, systemic, autoimmune disease that leads to excessive joint inflammation and is associated with significant morbidity and mortality. Although much is still to be learned about the aetiology RA, a growing body of evidence suggests that an altered vascular environment is an important aspect of its pathophysiology. In this context, RA shares many similarities with cancer, and it is expected that several angiogenic targets in cancer might be relevant to the treatment of RA. Here, we discuss how these targets can be combined with advances in drug development to generate the next generation of RA therapeutics.
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