Abstract
Purpose: Hallmark of the osteoarthritis (OA) disease pathophysiological process is the recuperation of OA chondrocytes towards a hypertrophic, growth plate-like morphology and signalling, leading to cartilage degeneration and mineralization. Previously, our group showed by genetics and functional studies that upregulation of thyroid signalling (T3) induces this process and results in an upregulation of known hypertrophic genes such as MMP13, COL1A1, COL10A1 and ALPL. Defining the underlying molecular pathways involved in T3 induced hypertrophy could yield potential markers of hypertrophy and druggable targets.
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