核因子卡帕B在椎间盘中的过度激活导致巨细胞的招募和严重的磁盘退化
bioRxiv : the preprint server for biology
|August 23, 2023
概括
在椎间盘 (IVD) 中过度活跃的核因子kappa B (NF-κB) 信号通过增加炎症和代谢因素驱动退化. 解决炎症的巨细胞可以减轻这些影响,为腰部疼痛提供潜在的治疗途径.
科学领域:
- 生物医学研究的研究.
- 分子生物学分子生物学
- 病理学 病理学 病理学
背景情况:
- 腰部疼痛 (LBP) 是导致残疾的主要原因,主要与椎间盘退化 (DD) 有关.
- 核因子kappa B (NF-κB) 是关键的炎症调节剂,与肌肉骨疾病有关,但其在DD中的直接作用尚不清楚.
结论:
- 长时间的NF-κB激活会通过调节炎症媒介,代谢酶和炎症巨细胞来诱导严重的DD.
- 来自炎症溶解巨细胞的分泌因子可以抵消DD中NF-κB过度激活的有害影响.
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