Integrative Multi‐Omics Analysis Identifies <scp>FTO</scp> as a Genetic and Epigenetic Link Between Metabolic Susceptibility and <i>Staphylococcus aureus</i> ‐Induced Airway Remodeling in Chronic Rhinosinusitis

A demethylase to stabilize the Metastasis Associated Lung Adenocarcinoma Transcript 1 (MALAT1). This molecular axis suppresses GSK-3β and promotes β-catenin nuclear translocation, thereby driving epithelial-mesenchymal transition (EMT) and pathological mucosal remodeling. By mapping the FTO-MALAT1-GSK-3β/β-catenin signaling network, this research elucidates how metabolic susceptibility facilitates infection-triggered epithelial reprogramming. These findings establish FTO as a promising biomarker and potential therapeutic target, providing a systemic foundation for personalized CRS treatment strategies.