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However, it is widely accepted that HO-1 is a heat shock protein that is controlled by inflammatory or pro-oxidant states and is induced in various pathologies in response to oxidative stress [1]

Cytokines and other inflammatory mediators initiate cascades that contribute to the perpetuation of inflammation, synovial hyperplasia, hypoxia, subsequent synovial angiogenesis, progressive joint degradation, the activation of fibroblasts and their transition to myofibroblasts

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Kobayashi H, Yamada Y, Kanayama S, Furukawa N, Noguchi T, Haruta S, Yoshida S, Sakata M, Sado T, Oi H

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