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利用脂肪组织来源干细胞的小细胞外囊泡靶向肌肉再生——综述

Targeting Muscle Regeneration with Small Extracellular Vesicles from Adipose Tissue-Derived Stem Cells-A Review.

作者信息

Laurindo Lucas Fornari, Lima Enzo Pereira de, Araújo Adriano Cressoni, Dogani Rodrigues Victória, Dias Jefferson Aparecido, Barbosa Tavares Filho Marcos, Zuccari Debora Aparecida Pires de Campos, Fornari Laurindo Lívia, Miglino Maria Angélica, Chagas Eduardo Federighi Baisi, Gregório Mendes Claudemir, Direito Rosa, Valenti Vítor Engrácia, Barbalho Sandra Maria

机构信息

Department of Biochemistry and Pharmacology, School of Medicine, Universidade de Marília (UNIMAR), Marília 17525-902, SP, Brazil.

Laboratory for Systematic Investigations of Diseases, Department of Biochemistry and Pharmacology, School of Medicine, Universidade de Marília (UNIMAR), Marília 17525-902, SP, Brazil.

出版信息

Cells. 2025 May 9;14(10):683. doi: 10.3390/cells14100683.

DOI:10.3390/cells14100683
PMID:40422186
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12110158/
Abstract

Extracellular vesicles (EVs) are membrane-bound structures released by cells carrying diverse biomolecules involved in intercellular communication. Small EVs are abundant in body fluids, playing a key role in cell signaling. Their natural occurrence and therapeutic potential, especially in the context of muscular disorders, make them a significant area of research. Sarcopenia, characterized by progressive muscle fiber loss, represents a pathological state in which EVs could offer therapeutic benefits, reducing morbidity and mortality. Recent studies have proposed an interplay between adipose tissue (AT) and skeletal muscle regarding sarcopenia pathology. AT dysregulation, as seen in obesity, contributes to skeletal muscle loss in a multifactorial way. While AT-derived stem cell (ATDSC) small EVs have been implicated in musculoskeletal homeostasis, their precise action in muscle regeneration remains incompletely understood. In this context, ATDSC-derived small EVs can stimulate skeletal muscle regeneration through improved proliferation and migration of muscle cells, enhancement of muscular perfusion, improvement of tendon and nerve regeneration, stimulation of angiogenesis, and promotion of myogenic differentiation. However, they can also increase skeletal muscle loss. Notably, this is the first comprehensive review to systematically examine the role of ATDSC-derived small EVs in sarcopenia.

摘要

细胞外囊泡(EVs)是细胞释放的膜结合结构,携带参与细胞间通讯的多种生物分子。小细胞外囊泡在体液中含量丰富,在细胞信号传导中起关键作用。它们的天然存在和治疗潜力,特别是在肌肉疾病方面,使其成为一个重要的研究领域。肌肉减少症以进行性肌纤维丢失为特征,是一种细胞外囊泡可能具有治疗益处、降低发病率和死亡率的病理状态。最近的研究提出了脂肪组织(AT)和骨骼肌在肌肉减少症病理方面的相互作用。肥胖中所见的脂肪组织失调以多因素方式导致骨骼肌丢失。虽然脂肪组织来源的干细胞(ATDSC)小细胞外囊泡与肌肉骨骼稳态有关,但其在肌肉再生中的精确作用仍不完全清楚。在这种情况下,脂肪组织来源的干细胞小细胞外囊泡可以通过改善肌肉细胞的增殖和迁移、增强肌肉灌注、改善肌腱和神经再生、刺激血管生成以及促进肌源性分化来刺激骨骼肌再生。然而,它们也会增加骨骼肌丢失。值得注意的是,这是第一篇系统研究脂肪组织来源的干细胞小细胞外囊泡在肌肉减少症中作用的综合综述。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4262/12110158/2187ab52f94e/cells-14-00683-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4262/12110158/29f725fc361f/cells-14-00683-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4262/12110158/2187ab52f94e/cells-14-00683-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4262/12110158/29f725fc361f/cells-14-00683-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4262/12110158/2187ab52f94e/cells-14-00683-g002.jpg

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Muscle Contraction Is Essential for Tendon Healing and Muscle Function Recovery After Achilles Tendon Rupture and Surgical Repair.肌肉收缩对于跟腱断裂和手术修复后的肌腱愈合及肌肉功能恢复至关重要。
J Orthop Res. 2025 Apr;43(4):746-755. doi: 10.1002/jor.26044. Epub 2025 Jan 12.
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Extracellular vesicles, RNA sequencing, and bioinformatic analyses: Challenges, solutions, and recommendations.
细胞外囊泡、RNA测序与生物信息学分析:挑战、解决方案及建议
J Extracell Vesicles. 2024 Dec;13(12):e70005. doi: 10.1002/jev2.70005.
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Minimal Information for Studies of Extracellular Vesicles (MISEV): Ten-Year Evolution (2014-2023).细胞外囊泡研究的最低限度信息(MISEV):十年演变(2014 - 2023年)
Pharmaceutics. 2024 Oct 29;16(11):1394. doi: 10.3390/pharmaceutics16111394.
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Mechanisms of muscle cells alterations and regeneration decline during aging.肌肉细胞在衰老过程中改变和再生能力下降的机制。
Ageing Res Rev. 2024 Dec;102:102589. doi: 10.1016/j.arr.2024.102589. Epub 2024 Nov 19.
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