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 (749 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
Enlargement of air spaces distal to the terminal bronchioles where gas-exchange normally takes place. This is usually due to destruction of the alveolar wall. Pulmonary emphysema can be classified by the location and distribution of the lesions.
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: Emphysema, Pulmonary; Emphysemas, Pulmonary; Pulmonary Emphysemas; Centriacinar Emphysema; Centriacinar Emphysemas; Emphysema, Centriacinar; Emphysemas, Centriacinar; Centrilobular Emphysema.
Where it fits in the MeSH classification
- Broader topics
- Pulmonary Disease, Chronic Obstructive
Related concepts
Research landscape
PubMed indexes 17,381 records tagged with the MeSH heading “Pulmonary Emphysema” (counts retrieved 2026-11-04). 1,514 of them (8.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 11,385 records.
Reviews account for 1,588 records (9.1%) and meta-analyses for 47. Randomized controlled trials number 185 (1.1%) 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 | 11,385 |
| 2000-2009 | 1,891 |
| 2010-2019 | 2,591 |
| 2020 onward | 1,514 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,588 | 9.1% |
| Meta-analyses | 47 | 0.3% |
| Randomized controlled trials | 185 | 1.1% |
Method: PubMed query "Pulmonary Emphysema"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in respiratory medicine
Research on airway and lung disease mixes lung-function tests, symptom diaries, imaging and hospital records, so what was measured and in whom matters as much as the result. Many conditions here, such as asthma and COPD, vary between people and over time, and exposure studies (smoking, pollution, workplace dust) show association rather than proof of cause. Nothing on this page is advice about treatment or inhalers; anyone with breathing difficulty should seek care from a qualified clinician. Check how the condition was defined, the severity of the people studied and whether outcomes were symptoms, lung function or hospital admissions.
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 |
|---|---|---|---|---|
| Syndrome of Combined Pulmonary Fibrosis and Emphysema: An Official ATS/ERS/JRS/ALAT Research Statement | 2022 | Research article Design not recorded in structured metadata | 163 | cc by PMID 35969190 · DOI · PMC7615200 |
| Matrix Metalloproteinases in Chronic Obstructive Pulmonary Disease | 2023 | Review article Design not recorded in structured metadata | 96 | cc by PMID 36835197 · DOI · PMC9966421 |
| Clearance of senescent cells reverts the cigarette smoke-induced lung senescence and airspace enlargement in p16-3MR mice | 2023 | Research article Design not recorded in structured metadata | 48 | cc by PMID 37078230 · DOI · PMC10352560 |
| Functional Lung Imaging Identifies Peripheral Ventilation Changes in ꞵ-ENaC Mice | 2025 | Research article Design not recorded in structured metadata | 10 | cc by PMID 39998270 · DOI · PMC11965024 |
Syndrome of Combined Pulmonary Fibrosis and Emphysema: An Official ATS/ERS/JRS/ALAT Research Statement [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Background: The presence of emphysema is relatively common in patients with fibrotic interstitial lung disease.
- Closing excerpt
- Conclusions: This statement delineates the syndrome of CPFE and highlights research priorities.
- 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 (250 words)
Background: The presence of emphysema is relatively common in patients with fibrotic interstitial lung disease. This has been designated combined pulmonary fibrosis and emphysema (CPFE). The lack of consensus over definitions and diagnostic criteria has limited CPFE research. Goals: The objectives of this task force were to review the terminology, definition, characteristics, pathophysiology, and research priorities of CPFE and to explore whether CPFE is a syndrome. Methods: This research statement was developed by a committee including 19 pulmonologists, 5 radiologists, 3 pathologists, 2 methodologists, and 2 patient representatives. The final document was supported by a focused systematic review that identified and summarized all recent publications related to CPFE. Results: This task force identified that patients with CPFE are predominantly male, with a history of smoking, severe dyspnea, relatively preserved airflow rates and lung volumes on spirometry, severely impaired DlCO, exertional hypoxemia, frequent pulmonary hypertension, and a dismal prognosis. The committee proposes to identify CPFE as a syndrome, given the clustering of pulmonary fibrosis and emphysema, shared pathogenetic pathways, unique considerations related to disease progression, increased risk of complications (pulmonary hypertension, lung cancer, and/or mortality), and implications for clinical trial design. There are varying features of interstitial lung disease and emphysema in CPFE. The committee offers a research definition and classification criteria and proposes that studies on CPFE include a comprehensive description of radiologic and, when available, pathological patterns, including some recently described patterns such as smoking-related interstitial fibrosis. Conclusions: This statement delineates the syndrome of CPFE and highlights research priorities.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35969190 · DOI · PMC7615200
Matrix Metalloproteinases in Chronic Obstructive Pulmonary Disease [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Matrix metalloproteinases (MMPs) are proteolytic enzymes that degrade proteins of the extracellular matrix and the basement membrane.
- Closing excerpt
- Considering the importance of MMPs in COPD pathogenesis, we also discuss MMPs as potential targets for therapeutic intervention in COPD and present evidence from recent clinical trials in this regard.
- 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 (125 words)
Matrix metalloproteinases (MMPs) are proteolytic enzymes that degrade proteins of the extracellular matrix and the basement membrane. Thus, these enzymes regulate airway remodeling, which is a major pathological feature of chronic obstructive pulmonary disease (COPD). Furthermore, proteolytic destruction in the lungs may lead to loss of elastin and the development of emphysema, which is associated with poor lung function in COPD patients. In this literature review, we describe and appraise evidence from the recent literature regarding the role of different MMPs in COPD, as well as how their activity is regulated by specific tissue inhibitors. Considering the importance of MMPs in COPD pathogenesis, we also discuss MMPs as potential targets for therapeutic intervention in COPD and present evidence from recent clinical trials in this regard.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36835197 · DOI · PMC9966421
Clearance of senescent cells reverts the cigarette smoke-induced lung senescence and airspace enlargement in p16-3MR mice [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Cigarette smoke (CS) leads to increased oxidative stress, inflammation, and exaggerated senescence, which are involved in the pathogenesis of chronic obstructive pulmonary disease (COPD).
- Closing excerpt
- Overall, our data provide evidence for the role of lung cellular senescence on smoke exposure and clearance of senescent cells in p16-3MR mice in the reversal of COPD/emphysema pathology with a possibility of senolytics as therapeutic interventions in 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 (195 words)
Cigarette smoke (CS) leads to increased oxidative stress, inflammation, and exaggerated senescence, which are involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). While the role of cellular senescence in COPD is known, it is not clear if the removal of senescent cells could alleviate the disease symptoms. To test this, we used the novel mouse model-p16-3MR, and studied the effect of ganciclovir (GCV)-mediated removal of senescent cells after chronic CS (3 months) and environmental tobacco smoke (ETS) (6 months) exposure to CS. Our results showed the reversal of CS-induced cellular senescence on the clearance of p16+ senesced cells by GCV treatment. Interestingly, the clearance of p16+ senescent cells via GCV led to a decrease in the neutrophil counts in the BALF of GCV-treated CS-exposed p16-3MR mice, as well as reversal of CS-mediated airspace enlargement in p16-3MR mice. Mice exposed to low dose ETS caused insignificant changes in the SA-β-Gal+ senescent cells and airspace enlargement. Overall, our data provide evidence for the role of lung cellular senescence on smoke exposure and clearance of senescent cells in p16-3MR mice in the reversal of COPD/emphysema pathology with a possibility of senolytics as therapeutic interventions in COPD.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37078230 · DOI · PMC10352560
Functional Lung Imaging Identifies Peripheral Ventilation Changes in ꞵ-ENaC Mice [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Background and objectiveβ-ENaC-Tg mice serve as a relevant model of muco-obstructive lung disease and diffuse-type emphysema, with impaired mucociliary clearance, mucus obstruction, chronic airway inflammation, structural lung damage, and altered lung function.
- Closing excerpt
- ConclusionThis research highlights the utility of XV imaging in evaluating ventilation defects in the β-ENaC-Tg model and provides a comprehensive lung function analysis.
- 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 (179 words)
Background and objectiveβ-ENaC-Tg mice serve as a relevant model of muco-obstructive lung disease and diffuse-type emphysema, with impaired mucociliary clearance, mucus obstruction, chronic airway inflammation, structural lung damage, and altered lung function. The aim of this study was to undertake a comprehensive analysis of lung function and mechanics of the adult β-ENaC-Tg model.MethodsAdult β-ENaC-Tg and wild-type littermates underwent X-ray velocimetry (XV) scans using a Permetium XV scanner (4DMedical, Melbourne, Australia). For comparative lung mechanics, lung function assessments were conducted with a flexiVent system (SCIREQ, Montreal, Canada).ResultsXV imaging demonstrated elevated ventilation defect percentage, mean specific ventilation, and ventilation heterogeneity in β-ENaC-Tg mice. Spatial analysis of ventilation maps indicated increased ventilation variability in the peripheral lung regions, as well as an increased proportion of under-ventilated areas. The flexiVent analysis indicated that compared to wild types, β-ENaC-Tg mice have a significantly more compliant lungs with increased inspiratory capacity, reduced tissue elastance, and increased hysteresivity (heterogeneity), suggesting loss of parenchymal integrity.ConclusionThis research highlights the utility of XV imaging in evaluating ventilation defects in the β-ENaC-Tg model and provides a comprehensive lung function analysis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39998270 · DOI · PMC11965024
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 The pathology of chronic obstructive pulmonary disease [5]
- Research article Alpha1-Antitrypsin Deficiency [6]
- Research article The discovery of α1-antitrypsin and its role in health and disease [7]
- Research article Combined pulmonary fibrosis and emphysema syndrome: a review [8]
- Research article Molecular pathogenesis of emphysema [9]
- Research article The pathology of small airways disease in COPD: historical aspects and future directions [10]
References
- Cottin V, Selman M, Inoue Y, Wong AW, Corte TJ, Flaherty KR, et al.. Syndrome of Combined Pulmonary Fibrosis and Emphysema: An Official ATS/ERS/JRS/ALAT Research Statement. . 2022. PMID 35969190 · DOI · PMC7615200
- Christopoulou ME, Papakonstantinou E, Stolz D. Matrix Metalloproteinases in Chronic Obstructive Pulmonary Disease. . 2023. PMID 36835197 · DOI · PMC9966421
- Kaur G, Muthumalage T, Rahman I. Clearance of senescent cells reverts the cigarette smoke-induced lung senescence and airspace enlargement in p16-3MR mice. . 2023. PMID 37078230 · DOI · PMC10352560
- Reyne N, Smith R, Cmielewski P, Eikelis N, Eikelis N, Nilsen K, et al.. Functional Lung Imaging Identifies Peripheral Ventilation Changes in ꞵ-ENaC Mice. . 2025. PMID 39998270 · DOI · PMC11965024
- Hogg JC, Timens W. The pathology of chronic obstructive pulmonary disease. Annu Rev Pathol. 2009. PMID 18954287 · DOI
- Strnad P, McElvaney NG, Lomas DA. Alpha1-Antitrypsin Deficiency. N Engl J Med. 2020. PMID 32268028 · DOI
- Janciauskiene SM, Bals R, Koczulla R, Vogelmeier C, Köhnlein T, Welte T. The discovery of α1-antitrypsin and its role in health and disease. Respir Med. 2011. PMID 21367592 · DOI
- Jankowich MD, Rounds SIS. Combined pulmonary fibrosis and emphysema syndrome: a review. Chest. 2012. PMID 22215830 · DOI · PMC3251269
- Taraseviciene-Stewart L, Voelkel NF. Molecular pathogenesis of emphysema. J Clin Invest. 2008. PMID 18246188 · DOI · PMC2214683
- Higham A, Quinn AM, Cançado JED, Singh D. The pathology of small airways disease in COPD: historical aspects and future directions. Respir Res. 2019. PMID 30832670 · DOI · PMC6399904
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 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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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.