Airway Remodeling and Structural Changes in Asthma

Asthma is a chronic, heterogeneous respiratory disorder defined not only by reversible airway obstruction and inflammation but also by persistent alterations in airway architecture, collectively termed airway remodelling. These structural changes encompass subepithelial fibrosis, increased airway smooth muscle mass, mucous gland hyperplasia, epithelial injury and repair abnormalities, and enhanced microvascularity. Together, they contribute to fixed airflow limitation, bronchial hyper-responsiveness and accelerated decline in lung function. Remodelling arises from a complex interplay of chronic type 2 inflammation, mechanical stress during bronchoconstriction, genetic and epigenetic influences, and epithelial–mesenchymal cross-talk. Assessment relies on a combination of endobronchial biopsy, advanced imaging modalities and non-invasive biomarkers. A deeper understanding of the mechanisms driving remodelling has informed the development of targeted therapies aimed at preventing or reversing structural damage and improving long-term outcomes in people with asthma.

Research from Nature Portfolio

Recent studies have explored the relationship between non-invasive inflammatory biomarkers and airway structure. Advanced three-dimensional computed tomography analyses have revealed that the fraction of exhaled nitric oxide correlates significantly with bronchial wall thickening across multiple airway generations. This correlation persists independent of demographic and treatment variables, suggesting that routine measurement of exhaled nitric oxide may serve as a practical surrogate for detecting and monitoring airway remodelling in clinical practice.

Airway Remodeling and Structural Changes in Asthma publication trend

The graph below shows the total number of articles in airway remodeling and structural changes in asthma across all publications each year (not limited to Nature Index journals).

Technical terms

Airway remodelling: Structural alterations in bronchial walls—including fibrosis, smooth muscle hypertrophy and gland enlargement—that contribute to fixed airflow limitation.

Fraction of exhaled nitric oxide (FeNO): A non-invasive measure of airway inflammation that correlates with bronchial wall thickening and structural change.

Fibrocytes: Circulating progenitor cells that home to the lung and differentiate into fibroblasts, promoting extracellular matrix deposition.

Alarmin cytokines: Epithelial-derived mediators released upon barrier damage that initiate and amplify inflammatory and remodelling cascades.

Computed tomography (CT): Volumetric imaging technique used in vivo to quantify airway wall dimensions, luminal area and patterns of air trapping.

References

1. Airway remodelling in asthma and the epithelium: on the edge of a new era. European Respiratory Journal (2024).
2. CD147 induces asthmatic airway remodeling and activation of circulating fibrocytes in a mouse model of asthma. Respiratory Research (2024).
3. Relationship between fraction of exhaled nitric oxide and airway morphology assessed by three-dimensional CT analysis in asthma. Scientific Reports (2017).
4. Airway remodeling heterogeneity in asthma and its relationship to disease outcomes. Frontiers in Physiology (2023).