Airway Epithelial Remodeling in Asthma Pathogenesis
Summary
Airway epithelial remodelling in asthma pathogenesis encompasses dynamic structural and functional changes within the respiratory epithelial lining that both sustain and exacerbate chronic airway obstruction. In healthy airways, the epithelium forms a selective barrier that regulates mucociliary clearance and orchestrates innate immune responses. In asthma, repeated allergen or viral insult triggers dysregulated repair processes, leading to goblet cell hyperplasia, basement membrane thickening and epithelial-mesenchymal transition (EMT). Disruption of tight junctions and altered secretion of growth factors and cytokines—such as transforming growth factor-β, interleukin-33 and thymic stromal lymphopoietin—drive interactions with mesenchymal cells and immune populations. Subepithelial fibrosis and deposition of extracellular matrix components reduce tissue compliance, while changes in matrix stiffness feed back to epithelial cell phenotype via mechanotransduction pathways. Exosomes and microRNAs further propagate inflammatory signals across the airway wall, promoting type-2 polarisation and bronchial hyperresponsiveness. Together, these interconnected processes define a self-perpetuating cycle of remodelling, fuel persistent symptoms and limit reversibility of airflow obstruction, highlighting the epithelium as a critical locus for therapeutic intervention and biomarker discovery.
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Airway Epithelial Remodeling in Asthma Pathogenesis publication trend
The graph below shows the total number of articles in airway epithelial remodeling in asthma pathogenesis across all publications each year (not limited to Nature Index journals).
Technical terms
Epithelial-mesenchymal transition (EMT): A phenotypic switch in which epithelial cells lose polarity and adhesion to acquire mesenchymal characteristics, contributing to subepithelial fibrosis.
Exosomes: Small extracellular vesicles released by cells that carry proteins, lipids and nucleic acids, mediating intercellular communication.
Th2 inflammation: A type-2 immune response driven by cytokines such as IL-4, IL-5 and IL-13, promoting eosinophil recruitment and IgE production.
MicroRNA (miRNA): Short non-coding RNA molecules that regulate gene expression post-transcriptionally by targeting messenger RNA for degradation or translational repression.
Interleukin-33 (IL-33): A cytokine released by damaged epithelial cells that activates type-2 innate lymphoid cells and Th2 lymphocytes, amplifying allergic inflammation.
CD146: A cell surface adhesion molecule implicated in signalling pathways that induce EMT and contribute to tissue remodelling.
References
- Airway epithelial‐derived exosomes induce acute asthma exacerbation after respiratory syncytial virus infection. MedComm (2024).
- Epithelial-Mesenchymal Transition in Asthma Airway Remodeling Is Regulated by the IL-33/CD146 Axis. Frontiers in Immunology (2020).
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