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骨骼肌来源的外泌体的最新进展及其与其他组织的相互作用。

Recent Advances of Exosomes Derived from Skeletal Muscle and Crosstalk with Other Tissues.

机构信息

College of Animal Science and Technology, Southwest University, Chongqing 400715, China.

College of Food Science, Southwest University, Chongqing 400715, China.

出版信息

Int J Mol Sci. 2024 Oct 10;25(20):10877. doi: 10.3390/ijms252010877.

Abstract

Skeletal muscle plays a crucial role in movement, metabolism, and energy homeostasis. As the most metabolically active endocrine organ in the body, it has recently attracted widespread attention. Skeletal muscle possesses the ability to release adipocytokines, bioactive peptides, small molecular metabolites, nucleotides, and other myogenic cell factors; some of which have been shown to be encapsulated within small vesicles, particularly exosomes. These skeletal muscle exosomes (SKM-Exos) are released into the bloodstream and subsequently interact with receptor cell membranes to modulate the physiological and pathological characteristics of various tissues. Therefore, SKM-Exos may facilitate diverse interactions between skeletal muscle and other tissues while also serving as biomarkers that reflect the physiological and pathological states of muscle function. This review delves into the pivotal role and intricate molecular mechanisms of SKM-Exos and its derived miRNAs in the maturation and rejuvenation of skeletal muscle, along with their intercellular signaling dynamics and physiological significance in interfacing with other tissues.

摘要

骨骼肌在运动、代谢和能量平衡中起着至关重要的作用。作为体内最具代谢活性的内分泌器官,它最近引起了广泛关注。骨骼肌具有释放脂肪细胞因子、生物活性肽、小分子代谢物、核苷酸和其他肌源性细胞因子的能力;其中一些已被证明被包裹在小泡内,特别是外泌体。这些骨骼肌外泌体(SKM-Exos)被释放到血液中,并随后与受体细胞膜相互作用,调节各种组织的生理和病理特征。因此,SKM-Exos 可能促进骨骼肌与其他组织之间的多种相互作用,同时也作为反映肌肉功能生理和病理状态的生物标志物。本综述深入探讨了 SKM-Exos 及其衍生的 miRNAs 在骨骼肌成熟和再生中的关键作用和复杂分子机制,以及它们在与其他组织相互作用时的细胞间信号动力学和生理意义。

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Cytokines and exosomal miRNAs in skeletal muscle-adipose crosstalk.细胞因子和外泌体 miRNAs 在骨骼肌-脂肪串扰中的作用。
Trends Endocrinol Metab. 2023 Oct;34(10):666-681. doi: 10.1016/j.tem.2023.07.006. Epub 2023 Aug 18.

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