Hypoxia, mitochondrial dysfunction and synovial invasiveness in rheumatoid arthritis

Hypoxia, arising as a consequence of the increased cellular demand for oxygen during the inflammatory response, is a powerful trigger for the activation, proliferation and survival of endothelial cells and fibroblast-like synoviocytesImpaired mitochondrial function and oxidative damage caused by hypoxia further exacerbate the inflammatory response through metabolic perturbationHypoxia induces immune cell dysfunction, resulting in an altered metabolic profileThe hypoxic environment induces activation of a complex crosstalk of signalling pathways, providing a feedback loop leading to further activation and inflammationTargeting synovial metabolic pathways through inhibition of hypoxia-induced signalling pathways might have therapeutic benefit for rheumatoid arthritis and other inflammatory diseases