Fig. 5.

Proposed mechanism for 3-MST involvement in osteoarthritic joints. Firstly, reactive oxygen species such as H₂O₂ decrease 3-MST expression (Fig. 4a). 3-MST inhibition leads to decreased endogenous H₂S production (Fig. 3c) which favors increased chondrocyte calcification (Fig. 3a and d), and interleukin-6 secretion (Fig. 3b). An amplification loop exists between mineralization and interleukin-6, which triggers OA progression [9]. Finally, mineralization and interleukin-6 can also cause downregulation of 3-MST, leading to sustained deleterious signal towards disease progression