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禁食诱导肌肉缩期间的适应性抗氧化反应由ZEB1和ZEB2相反调节

Chiara Ninfali¹, Marlies Cortés¹, M C Martínez-Campanario¹

¹Group of Gene Regulation in Stem Cells, Cell Plasticity, Differentiation, and Cancer, Institute of Biomedical Research August Pi Sunyer (IDIBAPS), Barcelona 08036, Spain.

Proceedings of the National Academy of Sciences of the United States of America

|November 10, 2023

概括

细胞可塑性因子ZEB1和ZEB2控制着禁食期间的抗氧化反应. ZEB1保护肌肉免受氧化损伤和缩,而ZEB2则会加剧肌肉损伤和缩,这表明ZEB因子是治疗点.

科学领域:

细胞生物学细胞生物学
分子生物学分子生物学
身体生理学身体生理学

背景情况:

反应性氧物种 (ROS) 对于恒温至关重要,但需要抗氧化剂来中和以防止氧化损伤.
骨肌肉适应禁食需要复杂的调节机制,包括抗氧化剂反应.

研究的目的:

研究转录因子ZEB1和ZEB2在调节骨肌肉中对禁食的适应性抗氧化反应中的作用.
确定ZEB1和ZEB2在禁食期间对肌肉缩和线粒体功能的影响.

主要方法:

使用了转基因小鼠,骨肌纤维特异性删除了Zeb1或Zeb2.
在禁食小鼠中分析了ROS的产生,抗氧化剂反应,线粒体活性和肌肉缩.
向Zeb1缺乏的小鼠提供抗氧化剂CDDO-TFEA.

主要成果:

在禁食小鼠中,Zeb1的缺失增加了ROS的产生,并降低了抗氧化反应,而Zeb2的缺失没有这样的效果.
禁食期间ZEB1表达增加,防止肌肉缩并改善线粒体功能.
禁食期间ZEB2表达减少,导致肌肉缩和线粒体损伤恶化.
抗氧化剂治疗在Zeb1缺乏的小鼠中逆转了有害的表型.

结论:

在禁食期间,ZEB1和ZEB2相反地调节骨肌肉中的适应性抗氧化反应.
ZEB1对于保护肌肉免受禁食引起的氧化应激和缩至关重要.
在禁食期间,ZEB2会加剧肌肉缩和线粒体功能障碍.
ZEB因子代表了与氧化还原失衡相关的条件的潜在治疗点.

关键词:

这就是NRF2的NRF2.在ZEB1和ZEB2中,ZEB1和ZEB2分别为ZEB1和ZEB2.抗氧化剂反应的抗氧化剂反应肌肉缩肌肉缩肌肉缩有活性氧物种的反应性氧物种.

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