Striated muscle is a highly specialized collection of tissues with contractile properties that vary according to functional needs. Although muscle fiber types are established postnatally, lifelong plasticity facilitates stimulus-dependent adaptation. Functional adaptation requires molecular adaptation, which is partially provided by miRNA-mediated post-transcriptional regulation. miR-206 is a muscle-specific miRNA enriched in slow muscles. We investigated whether miR-206 drives the slow muscle phenotype or is merely an outcome. We found that miR-206 expression increases in both physiological (including female sex and endurance exercise) and pathological conditions (muscular dystrophy and adrenergic agonism) that promote a slow phenotype. Consistent with that observation, the slow soleus muscle of male miR-206-knockout mice displays a faster phenotype than wild-type mice. Moreover, left ventricles of male miR-206 knockout mice have a faster myosin profile, accompanied by dilation and systolic dysfunction. Thus, miR-206 appears to be necessary to enforce a slow skeletal and cardiac muscle phenotype and to play a key role in muscle sexual dimorphisms.

横纹肌是高度专业化的组织集合，其收缩特性根据功能需求而变化。尽管肌纤维类型是在出生后形成的，但终生的可塑性有利于刺激依赖性适应。功能适应需要分子适应，这部分是由 miRNA 介导的转录后调节提供的。miR-206 是一种富含于慢肌中的肌肉特异性 miRNA。我们研究了 miR-206 是否驱动慢肌表型，或者仅仅是一个结果。我们发现 miR-206 表达在生理状况（包括女性性行为和耐力运动）和病理状况（肌营养不良和肾上腺素能激动）下都会增加，从而促进缓慢表型。与该观察结果一致，雄性 miR-206 敲除小鼠的慢比目鱼肌表现出比野生型小鼠更快的表型。此外，雄性 miR-206 敲除小鼠的左心室具有更快的肌球蛋白分布，并伴有扩张和收缩功能障碍。因此，miR-206 似乎对于增强缓慢的骨骼肌和心肌表型以及在肌肉性别二态性中发挥关键作用是必要的。