In organisms from flies to mammals, the initial formation of a functional tendon is completely dependent on chemical signals from muscle (myokines). However, how myokines affect the maturation, maintenance, and regeneration of tendons as a function of age is completely unstudied. Here we discuss the role of four myokines - fibroblast growth factors (FGF), myostatin, the secreted protein acidic and rich in cysteine (SPARC), and miR-29 - in tendon development and hypothesize a role for these factors in the progressive changes in tendon structure and function as a result of muscle wasting (disuse, aging and disease). Because of the close relationship between mechanical loading and muscle and tendon regulation, disentangling muscle-tendon crosstalk from simple mechanical loading is experimentally quite difficult. Therefore, we propose an experimental framework that hopefully will be useful in demonstrating muscle-tendon crosstalk in vivo. Though understudied, the promise of a better understanding of muscle-tendon crosstalk is the development of new interventions that will improve tendon development, regeneration, and function throughout the lifespan.

中文翻译：

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肌肉萎缩期间的肌腱串扰

在从苍蝇到哺乳动物的生物体中，功能性肌腱的初始形成完全依赖于来自肌肉（肌动蛋白）的化学信号。然而，肌细胞因子如何影响肌腱的成熟、维持和再生作为年龄的函数是完全未经研究的。在这里，我们讨论了四种肌细胞因子——成纤维细胞生长因子 (FGF)、肌生长抑制素、酸性和富含半胱氨酸的分泌蛋白 (SPARC) 和 miR-29——在肌腱发育中的作用，并假设这些因子在肌腱的渐进性变化中的作用。肌肉萎缩（废用、衰老和疾病）导致的肌腱结构和功能。由于机械负荷与肌肉和肌腱调节之间的密切关系，从简单的机械负荷中解开肌肉-肌腱串扰在实验上是相当困难的。所以，我们提出了一个实验框架，有望在体内演示肌肉 - 肌腱串扰方面有用。尽管研究不足，但更好地理解肌肉-肌腱串扰的前景是开发新的干预措施，以改善肌腱的发育、再生和整个生命周期的功能。