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肥胖症中骨骼肌线粒体的生命周期。

The lifecycle of skeletal muscle mitochondria in obesity.

机构信息

Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.

Ottawa Institute of Systems Biology, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.

出版信息

Obes Rev. 2021 May;22(5):e13164. doi: 10.1111/obr.13164. Epub 2021 Jan 13.

Abstract

Skeletal muscle possesses dramatic metabolic plasticity that allows for the rapid adaptation in cellular energy transduction to meet the demands of the organism. Obesity elicits changes in skeletal muscle structure and function, resulting in the accumulation of intramuscular lipids. The accumulation of intramuscular lipids in obesity is associated with impaired skeletal muscle mitochondrial content and function. Mitochondria exist as a dynamic network that is regulated by the processes of biogenesis, fusion, fission, and mitophagy. In this review, we outline adaptations in molecular pathways that regulate mitochondrial structure and function in obesity. We highlight the emerging role of dysregulated skeletal muscle macroautophagy and mitochondrial turnover in obesity. Future research should further elucidate the role of mitophagy in observed reductions in mitochondrial content and function during obesity.

摘要

骨骼肌具有显著的代谢可塑性,能够快速适应细胞能量转导,以满足机体的需求。肥胖会引起骨骼肌结构和功能的变化,导致肌肉内脂质的积累。肥胖时肌肉内脂质的积累与骨骼肌线粒体含量和功能受损有关。线粒体作为一个动态网络存在,其过程受到生物发生、融合、分裂和自噬的调节。在这篇综述中,我们概述了调节肥胖中线粒体结构和功能的分子途径的适应性。我们强调了骨骼肌巨自噬和线粒体周转率失调在肥胖中的新兴作用。未来的研究应该进一步阐明自噬在肥胖过程中线粒体含量和功能下降中的作用。

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