Biomechanical signals inhibit IKK activity to attenuate NF‐κB transcription activity in inflamed chondrocytes

Abstract

These results indicate that the signals generated by cyclic tensile strain act at multiple sites within the NF-kappaB signaling cascade to inhibit IL-1beta-induced proinflammatory gene induction. Taken together, these findings provide insight into how biomechanical signals regulate and reduce inflammation, and underscore their potential in enhancing the ability of chondrocytes to curb inflammation in diseased joints.