Asthma, a chronic inflammatory airway disorder, remains a global therapeutic challenge due to its complex pathogenic mechanisms. HDM in asthmatic airways activates the NF-κB pathway, triggering aberrant upregulation of LncRNA-ATB in bronchial epithelial cells. Through FISH, qRT-PCR, and luciferase reporter assays, we confirmed LncRNA-ATB functions as a molecular sponge for miR-21, reducing free miR-21 levels and alleviating its translational repression on Rab9. Western blot and immunofluorescence demonstrated that elevated Rab9 induces Golgi fragmentation, further promoting bronchial epithelial cell barrier injury, apoptosis, and amplified airway inflammation. Notably, silencing LncRNA-ATB reversed miR-21 downregulation, Rab9 overexpression, and Golgi disruption, attenuating airway remodeling. Collectively, LncRNA-ATB/miR-21/Rab9 axis mediates Golgi dysfunction-driven epithelial injury, highlighting a potential therapeutic target for asthma.

Asthma, Golgi Fragmentation, LncRNA-ATB, miR-21, Rab9