Abstract
Purpose: Osteoarthritis (OA) is a chronic joint disease characterized by cartilage degradation, alterations in bone formation or subchondral bone remodeling and progressive synovial inflammation. Inflammatory signaling is involved in OA pathophysiology. The activation of the NF-κB pathway by pro-inflammatory cytokines is essential to induce various inflammation-related factors (MMPs, iNOS, IL-1β, TNF-α), which further activate the signaling cascade resulting in a major catabolic effect and subsequent OA progression.
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