Collao Nicolas, Farup Jean, De Lisio Michael
School of Human Kinetics, University of Ottawa, Ottawa, ON, Canada.
Department of Biomedicine, Aarhus University, Aarhus, Denmark.
Front Cell Dev Biol. 2020 Jan 28;8:9. doi: 10.3389/fcell.2020.00009. eCollection 2020.
Obesity is a major public health concern and is associated with decreased muscle quality (i.e., strength, metabolism). Muscle from obese adults is characterized by increases in fatty, fibrotic tissue that decreases the force producing capacity of muscle and impairs glucose disposal. Fibro/adipogenic progenitors (FAPs) are muscle resident, multipotent stromal cells that are responsible for muscle fibro/fatty tissue accumulation. Additionally, they are indirectly involved in muscle adaptation through their promotion of myogenic (muscle-forming) satellite cell proliferation and differentiation. In conditions similar to obesity that are characterized by chronic muscle degeneration, FAP dysfunction has been shown to be responsible for increased fibro/fatty tissue accumulation in skeletal muscle, and impaired satellite cell function. The role of metabolic stress in regulating FAP differentiation and paracrine function in skeletal muscle is just beginning to be unraveled. Thus, the present review aims to summarize the recent literature on the role of metabolic stress in regulating FAP differentiation and paracrine function in skeletal muscle, and the mechanisms responsible for these effects. Furthermore, we will review the role of physical activity in reversing or ameliorating the detrimental effects of obesity on FAP function.
肥胖是一个主要的公共卫生问题，并且与肌肉质量下降（即力量、新陈代谢）有关。肥胖成年人的肌肉特征是脂肪性、纤维化组织增加，这会降低肌肉产生力量的能力并损害葡萄糖代谢。成纤维/脂肪生成祖细胞（FAPs）是驻留在肌肉中的多能基质细胞，负责肌肉纤维/脂肪组织的积累。此外，它们通过促进成肌（肌肉形成）卫星细胞的增殖和分化间接参与肌肉适应。在以慢性肌肉退化为特征的类似肥胖的情况下，已表明FAP功能障碍是骨骼肌中纤维/脂肪组织积累增加和卫星细胞功能受损的原因。代谢应激在调节骨骼肌中FAP分化和旁分泌功能方面的作用才刚刚开始被揭示。因此，本综述旨在总结近期关于代谢应激在调节骨骼肌中FAP分化和旁分泌功能方面的作用以及这些作用背后机制的文献。此外，我们将综述体育活动在逆转或改善肥胖对FAP功能的有害影响方面的作用。
