Fucosyltransferases in asthma: regulators of epithelial dysfunction, senescence, and airway inflammation.

Glycosylation is a critical post-translational modification that regulates protein folding, stability, and cellular communication. Among glycan modifications, fucosylation, catalyzed by fucosyltransferases (FUTs), plays important roles in immune regulation, epithelial homeostasis, and host-pathogen interactions. Increasing evidence suggests that dysregulated fucosylation contributes to chronic inflammatory airway diseases, including asthma. Asthma is characterized by chronic airway inflammation, epithelial barrier dysfunction, mucus hypersecretion, and airway remodeling, processes that are increasingly associated with altered glycosylation patterns. Recent studies indicate that specific FUT isoforms regulate epithelial integrity, mucin glycosylation, immune-cell recruitment, and inflammatory signaling in asthma. Emerging evidence also suggests that FUT-mediated fucosylation may contribute to airway remodeling and cellular senescence; however, direct evidence for these mechanisms in asthma remains limited, and many insights are derived from related respiratory diseases and experimental models. This review summarizes current knowledge of the FUT family and critically evaluates the evidence linking aberrant fucosylation to asthma pathogenesis. We discuss the roles of FUTs in epithelial dysfunction, mucus secretion, immune regulation, airway remodeling, and cellular senescence, while distinguishing established asthma-specific findings from emerging mechanistic hypotheses. Finally, we highlight current challenges, future research directions, and the potential of FUT-targeted strategies for biomarker discovery and precision therapies in asthma.