Airway smooth muscle is best known for its role as an airway constrictor in diseases such as asthma. However, its function in lung development is debated. A prevalent model, supported by in vitro data, posits that airway smooth muscle promotes lung branching through peristalsis and pushing intraluminal fluid to branching tips. Here, we test this model in vivo by inactivating Myocardin, which prevented airway smooth muscle differentiation. We found that Myocardin mutants show normal branching, despite the absence of peristalsis. In contrast, tracheal cartilage, vasculature, and neural innervation patterns were all disrupted. Furthermore, airway diameter is reduced in the mutant, counter to the expectation that the absence of smooth muscle constriction would lead to a more relaxed and thereby wider airway. These findings together demonstrate that during development, while airway smooth muscle is dispensable for epithelial branching, it is integral for building the tracheal architecture and promoting airway growth.

气道平滑肌以其在诸如哮喘等疾病中的气道收缩作用而闻名。然而，其在肺发育中的功能尚有争议。一个流行的模型得到体外数据的支持，认为气道平滑肌通过蠕动促进肺分支，并将腔内液体推向分支尖端。在这里，我们通过灭活心肌素（可防止气道平滑肌分化）在体内测试该模型。我们发现心肌素尽管没有蠕动，突变体仍显示正常的分支。相反，气管软骨，脉管系统和神经神经支配模式均被破坏。此外，突变体中的气道直径减小，这与没有平滑肌收缩会导致更放松从而更宽的气道的预期相反。这些发现共同表明，在发育过程中，尽管气道平滑肌对于上皮分支是必不可少的，但它对于建立气管结构和促进气道生长是必不可少的。