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失落在翻译中:一个被忽视的mTOR点为淋巴管状菌病

Jilly F Evans^1,2, Francis X McCormack³, Nahum Sonenberg⁴

¹Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA jillyfevans@gmail.com.

European respiratory review : an official journal of the European Respiratory Society

|September 27, 2023

概括

淋巴结核病 (Lymphangioleiomyomatosis,简称LAM) 是一种罕见的女性肺部疾病. 针对mTORC1路径的目标

科学领域:

生物医学研究的研究.
分子生物学分子生物学
遗传学遗传学是一个

背景情况:

淋巴细胞结核病 (Lymphangioleiomyomatosis,简称LAM) 是一种女性的囊性肺病,由结核硬化综合体 (TSC) 基因突变引起.
这些突变影响了哺乳动物中的拉巴素复合体1 (mTORC1) 途径的标,该途径调节细胞生长和新陈代谢.
mTORC1的激活促进了合成细胞功能,主要是通过通过S6K1/S6和4E-BP1/eIF4E通路的mRNA翻译.

研究的目的:

审查mTORC1在LAM病变发生中的作用.
为了评估拉帕米辛 (西罗利斯) 在稳定LAM患者的肺功能方面的疗效.
建议针对mTORC1驱动的翻译启动作为LAM和其他mTORC1驱动疾病的低估的治疗策略.

主要方法:

审查关于LAM,TSC,mTORC1信号和拉巴胺的现有文献.
对拉巴胺素对mTORC1下游通路 (S6K1/S6和4E-BP1/eIF4E) 的作用机制的分析.
对LAM和相关疾病的治疗影响的讨论.

主要成果:

拉巴胺在一些LAM患者中稳定了肺功能,但在药物停止后,疾病进展往往会恢复.
拉巴胺在可容忍度下有效抑制S6K1/S6轴 (翻译延伸).
在这些度下,拉巴胺不会显著抑制4E-BP1/eIF4E轴 (转化启动).

结论:

拉帕素对mTORC1通路的差异性抑制表明存在潜在的治疗缺口.
针对mTORC1驱动的翻译启动是一个有希望的,但被低估的,LAM的治疗策略.
这一策略也可能适用于结核性硬化综合体 (TSC) 和由mTORC1过度激活驱动的其他疾病.

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