From:  Evidence-based answers to clinical controversies in the management of severe asthma

 Remodeling in SA

AspectDescriptionClinical relevance
Epithelial barrierDamaged epithelial barrier stimulates ECM production by airway epithelial and smooth muscle cells.Leads to subepithelial fibrosis and reduced airway compliance.
Subepithelial fibrosisIncreased deposition of ECM components, including fragmented and disorganized fibrillar collagen.Associated with asthma severity and inversely correlated with FEV1.
Airway smooth muscle (ASM)ASM cell hyperplasia and hypertrophy contribute to airway remodeling.ASM cells have proinflammatory and immunomodulatory functions.
Goblet cell metaplasiaOverexpression of inflammatory angiogenesis and goblet cell metaplasia.Leads to mucus hyperproduction and airway obstruction.
AngiogenesisOverexpression of vascular endothelial growth factor and basic fibroblast growth factor.Contributes to airway remodeling and inflammation.
Inflammatory cellsPersistent airway infiltration/activation of immune cells, including eosinophils.Contributes to airway alterations and fixed airflow obstruction.
Fibroblast-to-myofibroblast transition (FMT)Enhanced differentiation of bronchial fibroblasts into myofibroblasts induced by TGF-β.Key aspects of subepithelial fibrosis.
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ECM: extracellular matrix; SA: severe asthma; TGF: transforming growth factor