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Cartilage degradation refers to the progressive destruction of cartilage extracellular matrix due to an imbalance between anabolic (matrix building) and catabolic (matrix breakdown) processes in joint tissue. This process is multifactorial, driven by mechanical overload, inflammation, and altered chondrocyte metabolism. Key mediators include matrix metalloproteinases (MMPs), aggrecanases (ADAMTS-family enzymes), pro-inflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-α), and signaling disruptions affecting chondrocyte function. Cartilage degradation is central to diseases such as osteoarthritis, where loss of proteoglycans and collagen results in weakening of tissue structure, joint pain, and loss of mobility[1][2][3][4].
Drugs may act via inhibition of matrix-degrading enzymes (e.g., MMP inhibitors), cytokine antagonism (e.g., IL-1 blockers), or anabolic pathway enhancement (e.g., TGF-β, BMP analogs)[1][2][3][4].
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