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通过TRPM2-介导的前循环,通过-cGAS-STING-NF-κB通路促进骨关节炎中软骨细胞损伤

Kai Sun¹, Xiong Zhang¹, Liangcai Hou¹

¹Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.

Journal of advanced research

|November 6, 2024

概括

暂时受体潜力梅拉斯2 (TRPM2) 通过促进涉及 (Ca2+),线粒体DNA (mtDNA) 和NF-κB信号的病理反循环,加剧了骨关节炎 (OA). 抑制这个TRPM2-Ca2+轴为OA提供了一个潜在的治疗策略.

科学领域:

生物医学科学生物医学科学
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

骨关节炎 (OA) 是老年人残疾的主要原因,有效治疗方法有限.
暂时受体潜在拉斯2 (TRPM2) 离子通道在OA病变发生过程中的作用尚不清楚.

研究的目的:

为了阐明TRPM2在骨关节炎中的功能.
研究TRPM2-介导的OA进展背后的分子机制.
评估TRPM2作为OA的潜在治疗标.

主要方法:

在人类和小鼠OA软骨中分析了TRPM2表达.
在小鼠中使用TRPM2淘汰和过度表达模型,小鼠中介半月 (DMM) 诱导的OA不稳定.
在体外研究中涉及siRNA/等离子体介导的TRPM2调制在IL-1β刺激的红细胞中.
研究了信号通路,转录因子和Ca2+合的治疗效果.

主要成果:

在患者和小鼠的OA软骨中,TRPM2的表达升高.
缺乏TRPM2可以防止DMM诱导的OA,而过度表达会加剧它.
IL-1β通过NF-κB-p65通路对TRPM2进行上调,从而激活TRPM2-Ca2+-mtDNA-cGAS-STING-NF-κB轴.
用BAPTA-AM减弱的已建立的OA进行Ca2+化.

结论:

通过调解病理反循环,TRPM2在OA病变发生过程中发挥着关键作用.
已识别的TRPM2-Ca2+-mtDNA-cGAS-STING-NF-κB轴代表了OA的一个新途径.
针对这一轴,特别是TRPM2-Ca2+相互作用,有望开发新的OA疗法.

关键词:

离子是一种离子.冠状细胞是什么意思冠状细胞在 NF-κBB 中.骨关节炎是一种骨关节炎.TRPM2TRPM2TRPM2TRPM2TRPM2TRPM2TRPM2TRPM2TRPM2TRPM2TRPM2TRPM2TRPM2TRPM2TRPM2

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