通过抑制TRIB3/AKAP1介导的Drp1酸化失调和线粒体分裂,L- 氨酸减轻椎间盘退化

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¹Department of Spine Surgery, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou 510289, China; Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510289, China.

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概括

补充L- 氨酸 (L- arg) 显示了对椎间盘退化 (IDD) 的治疗潜力. 它通过调节TRIB3-AKAP1-PKA/Drp1 ((S656) 途径来缓解细胞损伤和退化,提供了一个有前途的治疗策略.

科学领域:

生物化学
细胞生物学
整形医学

背景情况:

椎间盘退化 (IDD) 是腰部疼痛的一个重要原因.
IDD的潜在机制包括细胞衰老,细胞外矩阵功能障碍和线粒体损伤.
需要进一步阐明L-氨酸 (L-arg) 代谢在IDD病变中的作用.

研究的目的:

研究L-阿尔金因 (L-arg) 在椎间盘退化 (IDD) 的治疗潜力.
阐明L-arg对IDD产生影响的潜在分子机制.
在体外和体内IDD模型中评估L-arg的疗效.

主要方法:

使用代谢学,L- arg量化和免疫组织化学分析了人体核脉 (NP) 样本.
在体外研究中,使用RNA测序,西斑和共免疫沉治疗的NP细胞.
在老鼠IDD模型中使用MRI和免疫组织化学评估了体内疗效.

主要成果:

严重退化的NP组织显示L- arg水平降低.
在NP细胞中,L- arg补充减少了细胞衰老,改善了细胞外基质完整性 (ACAN增加),增强了线粒体功能 (ATP增加).
在老鼠模型中L- arg减弱的磁盘退化和抑制的炎症诱导的Tribbles同位素3 (TRIB3) 表达.
在S656中保持Drp1酸化并抑制病理性线粒体裂变.

结论:

在椎间盘退化 (IDD) 方面,L- 氨酸 (L- arginine) 具有显著的治疗潜力.
通过TRIB3-AKAP1-PKA/Drp1 (S656) 信号通路抑制线粒体分裂和细胞衰老,L- arg可以缓解IDD.
这些发现强调了L-arg作为治疗IDD的有前途药物.

关键词:

一个AKAP1 阿尔金因细胞衰老椎间盘退化线粒体动力学其他:

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