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骨肌 HSF1 通过SIRT3-PGC1α轴缓解与年龄相关的缩症和线粒体功能下降

Jun Zhang¹, Min Hu¹, Xia Wu¹

¹Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, 200241, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|December 16, 2025

概括

热冲击因子1 (HSF1) 的下降有助于与年龄相关的肌肉损失 (肉症). 恢复HSF1增强了线粒体功能和肌肉健康,为肉症和代谢障碍提供了潜在的治疗点.

科学领域:

细胞生物学细胞生物学
分子生物学分子生物学
衰老的研究研究.

背景情况:

与年龄相关的sarcopenia涉及肌肉质量和力量的损失,影响老年人的健康.
热冲击因子1 (HSF1) 在肉症中的作用目前尚不清楚.
HSF1调节细胞应激反应.

研究的目的:

调查HSF1在与年龄相关的肉症中的作用.
探索HSF1影响骨肌肉功能的分子机制.
评估HSF1在肉症和代谢障碍中的治疗潜力.

主要方法:

在老年小鼠和人类肌肉中分析HSF1mRNA表达.
产生和分析HSF1肌肉特异性淘汰赛小鼠.
RNA测序 (RNA-seq) 和ChIP测序 (ChIP-seq) 用于识别HSF1目标.
关于HSF1过度表达及其影响的体内和体外研究.

主要成果:

在老年肌肉中,HSF1mRNA表达减少,与缩和线粒体基因相关.
在HSF1淘汰赛中,小鼠表现出严重的肌肉缩,耐力减弱和代谢受损.
HSF1过度表达改善了肌肉功能和代谢性能.
HSF1激活了Sirtuin 3 (SIRT3),它去乙PGC1α异型,增强了线粒体功能和肌肉缩.
HSF1诱导FNDC5/Irisin,促进组织的交叉语音.

结论:

HSF1在维持骨肌肉质量,功能和全身能量平衡方面发挥着至关重要的作用.
SIRT3-PGC1α信号通路是HSF1发挥其作用的关键机制.
HSF1代表了一种有前途的治疗标,用于对抗肉症和相关的代谢障碍.

关键词:

衰老的衰老衰老的衰老线粒体中的线粒体.肌肉缩肌肉缩肌肉缩氧化功能氧化功能这种类型的麻症是sarcopenia.

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