Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (646 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The structural changes in the number, mass, size and/or composition of the airway tissues.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Airway Remodelings; Remodeling, Airway; Remodelings, Airway; Airway Remodelling; Airway Remodellings; Remodelling, Airway; Remodellings, Airway; Airway Wall Remodelling.
Where it fits in the MeSH classification
- Broader topics
- Pathological Conditions, Anatomical; Respiratory Physiological Phenomena
Research landscape
PubMed indexes 2,634 records tagged with the MeSH heading “Airway Remodeling” (counts retrieved 2026-10-31). 942 of them (35.8%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 1,663 records.
Reviews account for 549 records (20.8%) and meta-analyses for 2. Randomized controlled trials number 23 (0.9%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 70 |
| 2010-2019 | 1,663 |
| 2020 onward | 942 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 549 | 20.8% |
| Meta-analyses | 2 | 0.1% |
| Randomized controlled trials | 23 | 0.9% |
Method: PubMed query "Airway Remodeling"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| The pathology of small airways disease in COPD: historical aspects and future directions | 2019 | Review article Design not recorded in structured metadata | 184 | cc by PMID 30832670 · DOI · PMC6399904 |
| Spatial transcriptomics identifies molecular niche dysregulation associated with distal lung remodeling in pulmonary fibrosis | 2025 | Research article Design not recorded in structured metadata | 157 | cc by PMID 39901013 · DOI · PMC11906353 |
| Exhaled particles and small airways | 2019 | Review article Design not recorded in structured metadata | 129 | cc by PMID 30634967 · DOI · PMC6330423 |
| KCNJ2 is Required for NLRP3 Inflammasome Activation That Drives Allergic Airway Inflammation and Remodeling | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 41960844 · DOI · PMC13205818 |
The pathology of small airways disease in COPD: historical aspects and future directions [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Small airways disease (SAD) is a cardinal feature of chronic obstructive pulmonary disease (COPD) first recognized in the nineteenth century.
- Closing excerpt
- We discuss the need to specifically target SAD to attenuate the progression of COPD.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (123 words)
Small airways disease (SAD) is a cardinal feature of chronic obstructive pulmonary disease (COPD) first recognized in the nineteenth century. The diverse histopathological features associated with SAD underpin the heterogeneous nature of COPD. Our understanding of the key molecular mechanisms which drive the pathological changes are not complete. In this article we will provide a historical overview of key histopathological studies which have helped shape our understanding of SAD and discuss the hallmark features of airway remodelling, mucous plugging and inflammation. We focus on the relationship between SAD and emphysema, SAD in the early stages of COPD, and the mechanisms which cause SAD progression, including bacterial colonization and exacerbations. We discuss the need to specifically target SAD to attenuate the progression of COPD.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30832670 · DOI · PMC6399904
Spatial transcriptomics identifies molecular niche dysregulation associated with distal lung remodeling in pulmonary fibrosis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Large-scale changes in the structure and cellular makeup of the distal lung are a hallmark of pulmonary fibrosis (PF), but the spatial contexts that contribute to disease pathogenesis have remained uncertain.
- Closing excerpt
- Together, these results provide a unique, spatially resolved view of PF and establish methods that could be applied to other spatial transcriptomic studies.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (153 words)
Large-scale changes in the structure and cellular makeup of the distal lung are a hallmark of pulmonary fibrosis (PF), but the spatial contexts that contribute to disease pathogenesis have remained uncertain. Using image-based spatial transcriptomics, we analyzed the gene expression of 1.6 million cells from 35 unique lungs. Through complementary cell-based and innovative cell-agnostic analyses, we characterized the localization of PF-emergent cell types, established the cellular and molecular basis of classical PF histopathologic features and identified a diversity of distinct molecularly defined spatial niches in control and PF lungs. Using machine learning and trajectory analysis to segment and rank airspaces on a gradient of remodeling severity, we identified compositional and molecular changes associated with progressive distal lung pathology, beginning with alveolar epithelial dysregulation and culminating with changes in macrophage polarization. Together, these results provide a unique, spatially resolved view of PF and establish methods that could be applied to other spatial transcriptomic studies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39901013 · DOI · PMC11906353
Exhaled particles and small airways [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundOriginally, studies on exhaled droplets explored properties of airborne transmission of infectious diseases.
- Closing excerpt
- The biomarker potential is only at the beginning to be explored.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (186 words)
BackgroundOriginally, studies on exhaled droplets explored properties of airborne transmission of infectious diseases. More recently, the interest focuses on properties of exhaled droplets as biomarkers, enabled by the development of technical equipment and methods for chemical analysis. Because exhaled droplets contain nonvolatile substances, particles is the physical designation. This review aims to outline the development in the area of exhaled particles, particularly regarding biomarkers and the connection with small airways, i e airways with an internal diameter Main bodyGeneration mechanisms, sites of origin, number concentrations of exhaled particles and the content of nonvolatile substances are studied. Exhaled particles range in diameter from 0.01 and 1000 μm depending on generation mechanism and site of origin. Airway reopening is one scientifically substantiated particle generation mechanism. During deep expirations, small airways close and the reopening process produces minute particles. When exhaled, these particles have a diameter of ConclusionThe physical properties and content of exhaled particles generated by the airway reopening mechanism offers an exciting noninvasive way to obtain samples from the respiratory tract lining fluid of small airways. The biomarker potential is only at the beginning to be explored.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30634967 · DOI · PMC6330423
KCNJ2 is Required for NLRP3 Inflammasome Activation That Drives Allergic Airway Inflammation and Remodeling [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Airway inflammation and remodeling are cardinal features of asthma pathogenesis.
- Closing excerpt
- These results provide insight into the role of Kcnj2 in airway inflammation and remodeling in asthmatic conditions.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (184 words)
Airway inflammation and remodeling are cardinal features of asthma pathogenesis. Genome-wide association studies have shown that several SNPs of KCNJ2, a member of the inwardly rectifying potassium channel family, are associated with asthma in patients. However, the role of KCNJ2 in airway inflammation and remodeling in asthma remains unknown. Here, we demonstrate that the Kcnj2 serves as a critical regulator of airway epithelial inflammation and remodeling. KCNJ2 expression is significantly reduced in the airway epithelium of asthmatic patients, which is associated with goblet cell metaplasia and mucus overproduction. Epithelial cell depletion of Kcnj2 attenuates airway inflammation, Th2 inflammatory response, goblet cell metaplasia, and mucus overproduction in the airways of asthmatic mice. In cultured primary airway epithelial cells of asthmatic patients, KCNJ2 inhibition also hampers goblet cell metaplasia, mucus production, and lung epithelial cell-derived alarmins expression. This process appears to be mediated, at least in part, through inhibition of NLRP3 by restricting Ca2+ influx and K+ efflux, as pharmacological activation of NLRP3 diminishes the KCNJ2 inhibition-ameliorated airway phenotypes. These results provide insight into the role of Kcnj2 in airway inflammation and remodeling in asthmatic conditions.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41960844 · DOI · PMC13205818
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Role of chitin and chitinase/chitinase-like proteins in inflammation, tissue remodeling, and injury [5]
- Research article Airway basal stem cells: a perspective on their roles in epithelial homeostasis and remodeling [6]
- Research article Tuberculosis and lung damage: from epidemiology to pathophysiology [7]
- Research article The sentinel role of the airway epithelium in asthma pathogenesis [8]
- Research article Role of transforming growth factor-β in airway remodeling in asthma [9]
- Research article Remodeling in asthma [10]
References
- Higham A, Quinn AM, Cançado JED, Singh D. The pathology of small airways disease in COPD: historical aspects and future directions. . 2019. PMID 30832670 · DOI · PMC6399904
- Vannan A, Lyu R, Williams AL, Negretti NM, Mee ED, Hirsh J, et al.. Spatial transcriptomics identifies molecular niche dysregulation associated with distal lung remodeling in pulmonary fibrosis. . 2025. PMID 39901013 · DOI · PMC11906353
- Bake B, Larsson P, Ljungkvist G, Ljungström E, Olin AC. Exhaled particles and small airways. . 2019. PMID 30634967 · DOI · PMC6330423
- Cui Y, Wu S, Peng Y, Liu Y, Che L, Chen S, et al.. KCNJ2 is Required for NLRP3 Inflammasome Activation That Drives Allergic Airway Inflammation and Remodeling. . 2026. PMID 41960844 · DOI · PMC13205818
- Lee CG, Da Silva CA, Dela Cruz CS, Ahangari F, Ma B, Kang MJ, et al.. Role of chitin and chitinase/chitinase-like proteins in inflammation, tissue remodeling, and injury. Annu Rev Physiol. 2011. PMID 21054166 · DOI · PMC3864643
- Rock JR, Randell SH, Hogan BL. Airway basal stem cells: a perspective on their roles in epithelial homeostasis and remodeling. Dis Model Mech. 2010. PMID 20699479 · DOI · PMC2931533
- Ravimohan S, Kornfeld H, Weissman D, Bisson GP. Tuberculosis and lung damage: from epidemiology to pathophysiology. Eur Respir Rev. 2018. PMID 29491034 · DOI · PMC6019552
- Holgate ST. The sentinel role of the airway epithelium in asthma pathogenesis. Immunol Rev. 2011. PMID 21682747 · DOI
- Halwani R, Al-Muhsen S, Al-Jahdali H, Hamid Q. Role of transforming growth factor-β in airway remodeling in asthma. Am J Respir Cell Mol Biol. 2011. PMID 20525803 · DOI
- Al-Muhsen S, Johnson JR, Hamid Q. Remodeling in asthma. J Allergy Clin Immunol. 2011. PMID 21636119 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.