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通过DDIT3介导的线粒体细胞分裂,由质突巨细胞释放的线粒体DNA会加剧骨关节炎的进展

Chang Yang^1,2, Jin Ke¹, Qiongdong Xu¹

¹State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, 430079, China.

Journal of orthopaedic translation

|March 16, 2026

概括

线粒体DNA (mtDNA) 释放的pyroptotic synovial巨细胞驱动骨关节炎 (OA) 的进展. 以叶酸修饰的纳米颗粒向巨细胞灭,为OA治疗提供了一个潜在的治疗策略.

科学领域:

免疫学免疫学免疫学
生物化学生物化学
生物医学工程生物医学工程

背景情况:

骨关节炎 (OA) 涉及炎症性突巨细胞和受损的软骨细胞.
来自巨细胞的损伤相关分子模式 (DAMPs) 有助于OA中的细胞外基质 (ECM) 降解.

研究的目的:

为了研究炎症性突巨细胞中的DAMP如何促进红细胞中的ECM降解.
探索抵消OA中这些有害影响的策略.

主要方法:

在人类和小鼠OA中鉴定了突性巨细胞灭.
通过细胞和动物模型,研究了由热性巨细胞释放的线粒体DNA (mtDNA) 在ECM降解和软骨退化中的作用.
在体内评估了叶酸修饰的多聚乳糖糖酸 (PLGA) 纳米颗粒的治疗效果.

主要成果:

突性巨细胞中的线粒体功能障碍释放mtDNA,促进热致死并创造一种对OA软骨有害的炎症环境.
由于DDIT3缺乏,它通过PINK1/帕金基依赖性线粒细胞分裂抑制了线粒体的活性氧物种 (mtROS) 生产,从而减少了mtDNA释放和巨细胞的灭.
在体内,DDIT3缺乏和纳米颗粒治疗缓解了突炎症和软骨退化.

结论:

通过DDIT3介导的线粒细胞衰变,由皮罗普托斯结膜巨细胞释放的mtDNA在OA中起着病理作用.
叶酸修饰的PLGA纳米颗粒在提供治疗性药物治疗OA方面是有效的.

关键词:

软骨的退化软骨的退化在DDIT3中,DDIT3就是DDIT3 骨关节炎是一种骨关节炎.热性巨细胞的巨细胞.释放mtDNA的时间

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