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缺少MINK1刺激细胞核的细胞核灭,并加剧椎间盘退化

Kunyu Zhan¹, Keying Zhu¹, Bingyan Gu²

¹Institute of Orthopaedic and Traumatology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Traditional Chinese Medicine); The First Clinical College of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China; The Second Clinical College of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.

International immunopharmacology

|May 9, 2024

概括

形/Nck相互作用激酶 (NIK) 相关的激酶1 (MINK1) 衰减与椎间盘 (IVD) 退化相关. 由于MINK1缺失通过NF-κB信号传递促进细胞核热,从而加剧IVD退化,这表明MINK1是治疗标.

科学领域:

生物医学科学生物医学科学
细胞生物学细胞生物学
整形外科整形外科整形外科

背景情况:

椎间盘 (IVD) 退化会导致慢性腰部疼痛,其中核脉 (NP) 炎与其致病症有关.
在IVD退行症中NP热的调节机制尚未完全理解.
形/Nck交互激酶 (NIK) 相关的激酶1 (MINK1) 可能调节NLRP3炎症酶激活和烧灭.

研究的目的:

调查MINK1在细胞核核灭和椎间盘退化中的作用.
为了确定MINK1表达和IVD退化的严重程度之间的相关性.
阐明MINK1影响IVD退行的分子机制.

主要方法:

来自不同程度的IVD退化患者的NP组织的分析.
评估因衰老和腰椎不稳定性 (LSI) 的老鼠模型的IVD退化,有或没有MINK1切除.
对矩阵降解,NP热和NF-κB信号激活的评估.

主要成果:

在患者和小鼠模型中,MINK1表达在NP组织中减少,而IVD变性逐渐恶化.
在机械应激的小鼠中,MINK1切除显著增加了NP热,加速了细胞外基质 (ECM) 退化,并加剧了退化.
发现MINK1缺乏会激活NP组织中的NF-κB信号.

结论:

MINK1的表达与IVD退行症的严重程度相反相关.
缺少MINK1促进NP热,并通过激活NF-κB信号来加剧IVD退化.
MINK1代表了治疗椎间盘退行症的潜在治疗标.

关键词:

椎间盘退化椎间盘退化在 MINK1 上,你会看到 MINK1 .在NF-κB信号传输中.它的核心是脉的.热性灭症 (Pyroptosis) 是一种

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