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Herein, OA is a prime example of stress-associated joint disorder due to the constant and intense mechanical strain on the joints ( The aim of this review is, therefore, to (i) briefly summarize current knowledge on the pathogenesis of OA focusing on the (patho-)physiology of the synovial tissue, (ii) provide an overview of possible mechanisms of fibroblast to myofibroblast transformation in OA and (iii) outlines their metabolic alterations that improve our understanding of new potential therapeutic targets
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