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<p>Osteoarthritis (OA), a widespread form of degenerative joint disorder, is characterized by the gradual deterioration of articular cartilage.Serving as a versatile signaling mediator, tumor necrosis factor receptor-associated factor 6 (TRAF6) plays a key role in regulating cartilage matrix metabolism by controlling inflammatory mediators. This investigation examines the TRAF6/SPP1 pathway’s dual role in cartilage matrix remodeling during OA pathogenesis. Through integrated approaches including in vitro chondrocyte models, gene manipulation techniques, molecular assays (qRT-PCR, Western blot), and preclinical animal studies, we establish that TRAF6-mediated upregulation of secreted phosphoprotein 1 (SPP1) drives both matrix degradation and repair mechanisms in OA joints. Experimental evidence further demonstrates SPP1’s capacity to modulate chondrocyte-specific genetic markers, thereby influencing tissue degeneration and regenerative processes. These results elucidate the central regulatory mechanism of the TRAF6/SPP1 signaling cascade in OA pathophysiology.</p>

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The TRAF6/SPP1 axis participates in osteoarthritis progression through regulating the catabolism and anabolism of cartilage matrix

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月4日

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  • Jiapei Yao,
  • Jiliu Huang,
  • Chongrui Li,
  • JingJing Shang,
  • Xiaolong Lin,
  • Xindie Zhou,
  • Yaojun Lu

摘要

Osteoarthritis (OA), a widespread form of degenerative joint disorder, is characterized by the gradual deterioration of articular cartilage.Serving as a versatile signaling mediator, tumor necrosis factor receptor-associated factor 6 (TRAF6) plays a key role in regulating cartilage matrix metabolism by controlling inflammatory mediators. This investigation examines the TRAF6/SPP1 pathway’s dual role in cartilage matrix remodeling during OA pathogenesis. Through integrated approaches including in vitro chondrocyte models, gene manipulation techniques, molecular assays (qRT-PCR, Western blot), and preclinical animal studies, we establish that TRAF6-mediated upregulation of secreted phosphoprotein 1 (SPP1) drives both matrix degradation and repair mechanisms in OA joints. Experimental evidence further demonstrates SPP1’s capacity to modulate chondrocyte-specific genetic markers, thereby influencing tissue degeneration and regenerative processes. These results elucidate the central regulatory mechanism of the TRAF6/SPP1 signaling cascade in OA pathophysiology.