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However, the cellular and molecular mechanisms underlying tracheal SM formation remain poorly understood. Here, it is shown that the T\u2010type calcium channel CACNA1H is a novel regulator of tracheal SM formation and contraction. <jats:italic>Cacna1h<\/jats:italic> in an ethylnitrosourea forward genetic screen for regulators of respiratory disease using the mouse as a model is identified. <jats:italic>Cacna1h<\/jats:italic> mutants exhibit tracheal stenosis, disorganized SM and compromised tracheal contraction. CACNA1H is essential to maintain actin polymerization, which is required for tracheal SM organization and tube formation. This process appears to be partially mediated through activation of the actin regulator RhoA, as pharmacological increase of RhoA activity ameliorates the <jats:italic>Cacna1h<\/jats:italic>\u2010mutant trachea phenotypes. Analysis of human tracheal tissues indicates that a decrease in CACNA1H protein levels is associated with congenital tracheostenosis. These results provide insight into the role for the T\u2010type calcium channel in cytoskeletal organization and SM formation during tracheal tube formation and suggest novel targets for congenital tracheostenosis intervention.<\/jats:p>","DOI":"10.1002\/advs.202308622","type":"journal-article","created":{"date-parts":[[2024,10,3]],"date-time":"2024-10-03T06:40:02Z","timestamp":1727937602000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["The T\u2010Type Calcium Channel CACNA1H is Required for Smooth Muscle Cytoskeletal Organization During Tracheal Tubulogenesis"],"prefix":"10.1002","volume":"11","author":[{"given":"Ziying","family":"Liu","sequence":"first","affiliation":[{"name":"State Key Laboratory of Respiratory Disease National Clinical Research Center for Respiratory Disease Guangzhou Institute of Respiratory Health the First Affiliated Hospital of Guangzhou Medical University  Guangzhou Guangdong 510182 P. 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