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本文重点研究当前过氧化物酶体增殖物激活受体-γ辅激活因子1α(PGC-1α)调节通路的基本分子机制,并讨论日益增多的用线粒体生物发生补偿线粒体功能障碍和规避衰老及其相关疾病的可能疗效。PGC-1α是激发线粒体生物发生的主要转录调节因子,通过上调核呼吸因子(NRF-1,2)和线粒体转录因子A(Tfam),导致线粒体DNA复制和基因转录增加。PGC-1α还通过刺激对超氧化物歧化酶2(SOD2)、过氧化氢酶、谷胱甘肽过氧化物酶1(6PX1)、解偶联蛋白(UCP)的基因表达来调节细胞的氧化一抗氧化内稳定。最近关于肌肉特异性PGC-1α过表达的报告支持了PGC-1α在肌肉萎缩和少肌症中的益处,PGC-1α在过表达过程中能增强线粒体生物通路,减少氧化损伤。因此,PGC-1α似乎在抵抗衰老相关的骨骼肌退化中发挥重要保护作用。
This paper focuses on the current molecular mechanism of peroxisome proliferator activated receptor-γ-coactivator 1α (PGC-1α) regulatory pathways and discusses the increasing use of mitochondrial biogenesis to compensate for mitochondrial dysfunction and to circumvent it The possible effects of related diseases. PGC-1α is a major transcriptional regulator that stimulates mitochondrial biogenesis and upregulates mitochondrial DNA replication and gene transcription by upregulating nuclear respiration factor (NRF-1,2) and mitochondrial transcription factor A (Tfam). PGC-1α also regulates cell oxidation by stimulating the gene expression of superoxide dismutase 2 (SOD2), catalase, glutathione peroxidase 1 (6PX1) and uncoupling protein (UCP) An antioxidant stable. A recent report on muscle-specific PGC-1α overexpression supports the benefits of PGC-1α in muscle atrophy and sarcopenia, which enhances mitochondrial bio-pathways and reduces oxidative damage during overexpression. Therefore, PGC-1α appears to play an important protective role against aging-related skeletal muscle degeneration.