• CTNNAL1 is essential for maintaining airway epithelial structural integrity under ozone stress, as its knockdown leads to epithelial denudation and damage in mice.
• Silencing CTNNAL1 in human bronchial epithelial cells reduces proliferation and weakens cell-matrix and cell-cell adhesion, likely via cytoskeletal disruption.
• CTNNAL1 regulates the expression of adhesion molecules (E-cadherin, integrin β1, integrin β4) through the RhoA/ROCK1 signaling pathway.
• The ROCK inhibitor Y27632 reverses ozone-induced adhesion molecule expression in CTNNAL1-overexpressing cells, highlighting a potential therapeutic target for airway diseases.