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线粒体功能障碍相关的细胞衰老部分参与了小鼠的白素诱导的肺纤维化

Ya-Xin Yao¹, Xue Lu², Zhao Li¹

¹Department of Respiratory and Critical Care Medicine, the Second Affiliated Hospital of Anhui Medical University, Hefei 230601, Anhui, China.

Toxicology and applied pharmacology

|August 21, 2025

概括

通过诱导线粒体功能障碍和衰老,白素 (BLM) 导致肺纤维化. 用尼古丁胺单核酸 (NMN) 增强线粒体功能可能会防止这种纤维化.

科学领域:

肺部医学
细胞生物学
线粒体生物学

背景情况:

白素 (BLM) 是一种已知诱导肺间膜纤维化的抗瘤药物.
目前尚不完全了解BLM诱导的肺纤维化背后的确切机制.
线粒体功能障碍和细胞衰老与纤维化疾病有关.

研究的目的:

研究线粒体功能障碍相关的衰老在BLM诱导的肺纤维化中的作用.
探索NAD+前体对这一过程的潜在治疗效果.

主要方法:

成年C57BL/6J小鼠接受了BLM的治疗.
评估了表皮-介质细胞过渡 (EMT),细胞周期停止和与衰老相关的分泌表型 (SASP) 的标志物.
评估了线粒体形态,ATP含量和关键线粒体酶 (SOD2,IDH2).
通过基因淘汰对Sirtuin 3 (SIRT3) 的作用和尼古丁胺单核酸 (NMN) 治疗的影响进行了研究.

主要成果:

BLM治疗增加了EMT标志物 (α-SMA,Vimentin),原沉积,细胞循环停止标志物 (p16,p21) 和SASP指标.
由线粒体面积减少,ATP含量降低和SOD2/IDH2水平所证明的BLM诱导的线粒体功能障碍.
在接受BLM治疗的肺部中观察到SIRT3的降低.
Sirt3基因淘汰导致BLM诱导的肺纤维化和衰老.
在NMN前期治疗中减轻了BLM诱导的线粒体功能障碍,衰老,EMT和肺纤维化.

结论:

线粒体功能障碍相关的衰老在BLM诱导的肺纤维化中起着部分作用.
在这个过程中,SIRT3 是一个关键的调节器.
作为NAD+的前体,NMN通过向线粒体功能障碍和衰老来减轻BLM诱导的肺纤维化的治疗作用.

关键词:

布莱米辛与线粒体功能障碍相关的衰老尼古丁胺单核酸肺纤维化在SIRT3中

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