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PGC-1α-mediated regulation of mitochondrial function and physiological implications.
Applied Physiology, Nutrition, and Metabolism ( IF 2.4 ) Pub Date : 2020-06-09 , DOI: 10.1139/apnm-2020-0005
Jens Frey Halling 1, 1 , Henriette Pilegaard 1, 1
Affiliation  

Applied Physiology, Nutrition, and Metabolism, e-First Articles.
The majority of human energy metabolism occurs in skeletal muscle mitochondria emphasizing the importance of understanding the regulation of myocellular mitochondrial function. The transcriptional co-activator peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) has been characterized as a major factor in the transcriptional control of several mitochondrial components. Thus, PGC-1α is often described as a master regulator of mitochondrial biogenesis as well as a central player in regulating the antioxidant defense. However, accumulating evidence suggests that PGC-1α is also involved in the complex regulation of mitochondrial quality beyond biogenesis, which includes mitochondrial network dynamics and autophagic removal of damaged mitochondria. In addition, mitochondrial reactive oxygen species production has been suggested to regulate skeletal muscle insulin sensitivity, which may also be influenced by PGC-1α. This review aims to highlight the current evidence for PGC-1α-mediated regulation of skeletal muscle mitochondrial function beyond the effects on mitochondrial biogenesis as well as the potential PGC-1α-related impact on insulin-stimulated glucose uptake in skeletal muscle. Novelty PGC-1α regulates mitochondrial biogenesis but also has effects on mitochondrial functions beyond biogenesis. Mitochondrial quality control mechanisms, including fission, fusion, and mitophagy, are regulated by PGC-1α. PGC-1α-mediated regulation of mitochondrial quality may affect age-related mitochondrial dysfunction and insulin sensitivity.


中文翻译:

PGC-1α介导的线粒体功能调节及其生理意义。

《应用生理学,营养与代谢》,电子优先文章。
人类大部分能量代谢发生在骨骼肌线粒体中,强调了理解肌细胞线粒体功能调节的重要性。转录共激活因子过氧化物酶体增殖物激活的受体γ共激活因子1 alpha(PGC-1α)已被表征为几个线粒体组分转录控制的主要因素。因此,PGC-1α通常被描述为线粒体生物发生的主要调节剂,并且是调节抗氧化防御的重要角色。但是,越来越多的证据表明,PGC-1α还参与了生物合成以外的线粒体质量的复杂调控,其中包括线粒体网络动力学和自噬去除受损的线粒体。此外,线粒体活性氧的产生已被建议调节骨骼肌胰岛素敏感性,这也可能受到PGC-1α的影响。这篇综述旨在突出PGC-1α介导的骨骼肌线粒体功能调节的当前证据,而不仅仅是对线粒体生物发生的影响以及PGC-1α对胰岛素刺激骨骼肌摄取葡萄糖的潜在影响。新奇PGC-1α调节线粒体的生物发生,但对线粒体功能的影响超出生物发生。PGC-1α调节线粒体的质量控制机制,包括裂变,融合和线粒体吞噬。PGC-1α介导的线粒体质量调节可能影响与年龄有关的线粒体功能障碍和胰岛素敏感性。这也可能受到PGC-1α的影响。这篇综述旨在突出PGC-1α介导的骨骼肌线粒体功能调节的当前证据,而不仅仅是对线粒体生物发生的影响以及PGC-1α对胰岛素刺激骨骼肌摄取葡萄糖的潜在影响。新奇PGC-1α调节线粒体的生物发生,但对线粒体功能的影响超出生物发生。PGC-1α调节线粒体的质量控制机制,包括裂变,融合和线粒体吞噬。PGC-1α介导的线粒体质量调节可能影响与年龄有关的线粒体功能障碍和胰岛素敏感性。这也可能受到PGC-1α的影响。这篇综述旨在突出PGC-1α介导的骨骼肌线粒体功能调节的当前证据,而不仅仅是对线粒体生物发生的影响以及PGC-1α对胰岛素刺激骨骼肌摄取葡萄糖的潜在影响。新奇PGC-1α调节线粒体的生物发生,但对线粒体功能的影响超出生物发生。PGC-1α调节线粒体的质量控制机制,包括裂变,融合和线粒体吞噬。PGC-1α介导的线粒体质量调节可能影响与年龄有关的线粒体功能障碍和胰岛素敏感性。这篇综述旨在突出PGC-1α介导的骨骼肌线粒体功能调节的当前证据,而不仅仅是对线粒体生物发生的影响以及PGC-1α对胰岛素刺激骨骼肌摄取葡萄糖的潜在影响。新奇PGC-1α调节线粒体的生物发生,但对线粒体功能的影响超出生物发生。PGC-1α调节线粒体的质量控制机制,包括裂变,融合和线粒体吞噬。PGC-1α介导的线粒体质量调节可能影响与年龄有关的线粒体功能障碍和胰岛素敏感性。这篇综述旨在突出PGC-1α介导的骨骼肌线粒体功能调节的当前证据,而不仅仅是对线粒体生物发生的影响以及PGC-1α对胰岛素刺激骨骼肌摄取葡萄糖的潜在影响。新奇PGC-1α调节线粒体的生物发生,但对线粒体功能的影响超出生物发生。PGC-1α调节线粒体的质量控制机制,包括裂变,融合和线粒体吞噬。PGC-1α介导的线粒体质量调节可能影响与年龄有关的线粒体功能障碍和胰岛素敏感性。PGC-1α调节线粒体的质量控制机制,包括裂变,融合和线粒体吞噬。PGC-1α介导的线粒体质量调节可能影响与年龄有关的线粒体功能障碍和胰岛素敏感性。PGC-1α调节线粒体的质量控制机制,包括裂变,融合和线粒体吞噬。PGC-1α介导的线粒体质量调节可能影响与年龄有关的线粒体功能障碍和胰岛素敏感性。
更新日期:2020-06-09
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