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含有65个缺陷的三方基因通过减轻电压依赖的阳离子通道1介导的线粒体功能障碍来保护急性损伤

Tao Chen^1,2,3, Yang Zhang¹, Liting Ding²

¹Department of Anesthesiology, The First Affiliated Hospital, Jiangxi Medical College Nanchang University Nanchang China.

|April 23, 2025

概括

含有65 (TRIM65) 的三部分基因在急性损伤 (AKI) 中被上调. TRIM65缺乏通过稳定电压依赖性离子通道1 (VDAC1),防止线粒体功能障碍,从而防止AKI.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

急性损伤 (AKI) 是一种常见的临床疾病,患病率和死亡率很高.
目前对AKI的治疗策略是有限的,因为对其复杂病理学的理解不完全.
已知含有65 (TRIM65) 的三方基因调节炎症,但其在AKI中的作用尚未被探索.

研究的目的:

调查TRIM65在AKI病变发生中的作用.
阐明TRIM65影响AKI的分子机制.
探索TRIM65作为AKI的潜在治疗点.

主要方法:

在AKI模型中评估TRIM65表达.
使用TRIM65淘汰赛小鼠来评估其对各种AKI类型的保护作用 (狂腹肌溶解,缺血-再输液,西斯普拉丁诱导).
研究了TRIM65和电压依赖离子通道1 (VDAC1) 之间的相互作用,包括无处不在的位和对VDAC1稳定性和自的影响.
研究了TRIM65缺乏对管状上皮细胞中的线粒体功能的影响.
评估了VDAC1过度表达对AKI中TRIM65缺陷中介保护的影响.

主要成果:

在AKI中,TRIM65表达被发现是上调的.
TRIM65淘汰赛小鼠对多种形式的AKI显示出显著的保护.
确定TRIM65直接结合并调节K161和K200的VDAC1的多基化,增强VDAC1的稳定性并抑制其自降解.
在AKI期间,TRIM65缺乏改善了管细胞中的线粒体功能障碍.
过度表达VDAC1逆转了AKI中TRIM65缺乏的保护作用.

结论:

通过调节VDAC1稳定性和VDAC1依赖的线粒体功能,TRIM65在AKI发育中发挥着关键作用.
针对TRIM65-VDAC1轴为AKI提供了一个潜在的治疗策略.
对TRIM65和VDAC1的进一步研究可能会导致急性损伤的新治疗方法.

关键词:

急性损伤 (AKI) 是一种严重的损伤.线粒体功能障碍线粒体功能障碍包含65 (TRIM65) 的三部分图案无处不在的化电压依赖的离子通道1 (VDAC1)

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