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在肠道缺血-再输液损伤中,TRIM25通过线粒体DNA释放触发热致死 (pyroptosis)

Song Yao¹, Xiaolong Lu², Ximeng Ren¹

¹Department of Clinical Laboratory, the First Affiliated Hospital of Dalian Medical University, Dalian 116011, China; Department of Pharmacology, College of Pharmacy, Dalian Medical University, 9 West Section, Lvshun Road, Lvshunkou District, Dalian 116044, China.

Free radical biology & medicine

|February 12, 2026

概括

通过cGAS-STING通路激活NLRP3炎症体,TRIM25蛋白在再注射后触发肠道损伤. 针对这种途径可能为肠道缺血-再输液损伤提供新的治疗方法.

科学领域:

胃肠病学胃肠病学
免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

肠道缺血-反 (I/R) 损伤导致严重的炎症,缺乏有效的治疗方法.
NLRP3炎症酶激活是肠道I/R病原发生的一个关键因素.
需要澄清TRIM25在肠道I/R中的作用及其与NLRP3炎症酶激活的联系.

研究的目的:

研究TRIM25在肠道I/R中的作用.
阐明TRIM25影响NLRP3炎症酶激活的机制.
探索针对治疗干预的TRIM25中介途径的潜力.

主要方法:

在小鼠的肠道I / R和低氧-再氧化 (H / R) 模型中.
TRIM25的敲击和cGAS的抑制.
评估NLRP3炎症酶激活,cGAS-STING通路,线粒体功能和DNA释放.
同免疫沉以研究蛋白质相互作用.

主要成果:

在肠道I/R中,TRIM25的表达被上调,与NLRP3炎症酶激活相关.
TRIM25 Knockdown抑制了H/R诱导的NLRP3炎症酶和cGAS-STING通路的激活.
TRIM25与PGAM5相互作用,促进线粒体DNA释放和随后的cGAS-STING激活.

结论:

TRIM25通过通过PGAM5相互作用启动mtDNA释放,激活cGAS-STING通路,随后激活NLRP3炎症酶来驱动肠道I/R损伤.
针对TRIM25-PGAM5-mtDNA-cGAS-STING轴为肠道I / R提供了一个有希望的治疗策略.
这项研究揭示了一种新的分子机制,它是肠道I/R病原体的基础.

关键词:

肠道缺血-再输损伤 (I/R) 的原因热灭菌的发生.在cGAS-STING路径中.我们的mtDNA mtDNA

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