Non-canonical NF-κB signaling in endothelial cells may enhance synovial inflammation by stimulating angiogenesis

Pathological angiogenesis can be observed in rheumatoid arthritis (RA) synovial tissue (ST) already in the earliest phase of disease and may be critical in the switch from acute to chronic inflammation. The chemokine CXCL12 is regulated by non-canonical NF-κB signaling and stimulates angiogenesis in endothelial cells (EC). Therefore, the non-canonical NF-κB pathway, with its key mediator NF-κB inducing kinase (NIK), may play an important role in pathological angiogenesis leading to the perpetuation of synovial inflammation in RA. To study the role of non-canonical NF-κB signaling in pathological angiogenesis in RA.