Abstract
Purpose: While inflammation in osteoarthritis (OA) needs to be controlled to attenuate OA pathogenesis, maintenance of proper dynamics of chondrocyte physiology would also be critical to inhibit the onset and early progression of OA. Due to the complicated etiology of OA, there are no effective disease-modifying treatments to date, and significant unmet medical needs exist for a disease-modifying OA drug (DMOAD). Nkx3.2 was initially identified as a pro-chondrogenic factor promoting cartilage development.
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