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我认为P.P.是P.P. 牙周细胞通过依赖于线粒体裂变的VDAC1-HK2解离诱导内皮功能障碍

Yi Wang¹, Shengming Xu¹, Zichao Zhuang¹

¹Institute of Stomatology, School and Hospital of Stomatology, Wenzhou Medical University, Wenzhou, Zhejiang, People's Republic of China.

Journal of oral microbiology

|March 16, 2026

概括

Porphyromonas gingivalis 感染通过过度激活线粒体透性过渡孔 (mPTP) 来损害内皮细胞. 向与胺相关的蛋白1 (Drp1) 和mPTP开口可以恢复内皮功能并预防血管损伤.

科学领域:

心血管生物学心血管生物学
线粒体生物学线粒体生物学
牙周病的发病因子牙周病的发病因子

背景情况:

线粒体功能障碍是Porphyromonas gingivalis诱导的内皮损伤的一个关键因素.
线粒体透性过渡孔 (mPTP) 在维护线粒体平衡中起着至关重要的作用.
了解P. gingivalis对mPTP的影响对于解决相关的血管并发症至关重要.

研究的目的:

为了研究P. gingivalis是如何触发与胺相关蛋白1 (Drp1) 相关的mPTP过度激活的.
阐明将P. gingivalis感染与线粒体损伤和内皮功能障碍联系在一起的机制.
评估针对P. gingivalis相关的血管损伤的DRp1和mPTP的治疗潜力.

主要方法:

在感染P. gingivalis的人类大动脉内皮细胞和小鼠中评估了线粒体和内皮功能.
利用西式涂抹,免疫光和共同免疫沉来分析线粒体动力学和蛋白质相互作用.
在抑制Drp1和mPTP后检查了大动脉血管扩张和内皮完整性.

主要成果:

牙周杆菌感染导致线粒体碎片化,过度的mPTP开放,以及血管松功能受损.
观察到p-Drp1水平增加和线粒体转位.
P. gingivalis促进了DRp1介导的VDAC1寡合化,破坏了VDAC1-HK2的相互作用,并促进了mPTP的开放.

结论:

P. gingivalis通过Drp1-VDAC1-HK2介导的mPTP过度激活来损害内皮功能.
抑制Drp1和mPTP有效地恢复了线粒体和内皮的功能.
这一途径代表了在牙周感染中血管损伤的潜在治疗标.

关键词:

DRP1 是一个DRP1 内皮质功能障碍内皮质功能障碍葡萄牙牙牙病 Porphyromonas gingivalis 这种虫子是 mPTPTP 这是一个很好的方法.线粒体中的线粒体.

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