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<p>Lumbar Spinal Stenosis (LSS), a degenerative disorder, greatly impacts the elderly, often leads to discomfort, neurological problems, and a diminished quality of life. Ligamentum flavum hypertrophy (LFH), a marked influencor in LSS, is characterized by fibrosis resulting from excessive extracellular matrix deposition, largely driven by the differentiation of fibroblasts and inflammatory processes. Transforming growth factor β1 (TGF-β1) is pivotal in the LFH advancement by promoting fibrosis, highlighting its potential as a target for therapeutic strategies. Cartilage intermediate layer protein (CILP), known to regulate TGF-β1 activity in other tissues, may have potential in mitigating LFH. This research explores the function of CILP in LFH through the use of sophisticated bioinformatics, human samples, and experimental models, identifying its regulatory influence via the TGF-β1/SMAD3/SERPINE2 pathway.</p>

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Cartilage intermediate layer protein inhibits ligamentum flavum hypertrophy mediated by TGF-β1/SMAD3/SERPINE2 signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月9日

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  • Jiale Dong,
  • Peng Li,
  • Longxiao Wu,
  • Saifei Meng,
  • Guiwang Liu,
  • Xiaoming Chen,
  • Guiqing Wang,
  • Chunlei Liu

摘要

Lumbar Spinal Stenosis (LSS), a degenerative disorder, greatly impacts the elderly, often leads to discomfort, neurological problems, and a diminished quality of life. Ligamentum flavum hypertrophy (LFH), a marked influencor in LSS, is characterized by fibrosis resulting from excessive extracellular matrix deposition, largely driven by the differentiation of fibroblasts and inflammatory processes. Transforming growth factor β1 (TGF-β1) is pivotal in the LFH advancement by promoting fibrosis, highlighting its potential as a target for therapeutic strategies. Cartilage intermediate layer protein (CILP), known to regulate TGF-β1 activity in other tissues, may have potential in mitigating LFH. This research explores the function of CILP in LFH through the use of sophisticated bioinformatics, human samples, and experimental models, identifying its regulatory influence via the TGF-β1/SMAD3/SERPINE2 pathway.