Lung ageing and COPD: is there a role for ageing in abnormal tissue repair?
Open accessAbstract
Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death worldwide, with increasing prevalence, in particular in the elderly. COPD is characterised by abnormal tissue repair resulting in (small) airways disease and emphysema. There is accumulating evidence that ageing hallmarks are prominent features of COPD. These ageing hallmarks have been described in different subsets of COPD patients, in different lung compartments and also in a variety of cell types, and thus might contribute to different COPD phenotypes. A better understanding of the main differences and similarities between normal lung ageing and the pathology of COPD may improve our understanding of the mechanisms driving COPD pathology, in particular in those patients that develop the most severe form of COPD at a relatively young age, i.e. severe early-onset COPD patients. In this review, after introducing the main concepts of lung ageing and COPD pathology, we focus on the role of (abnormal) ageing in lung remodelling and repair in COPD. We discuss the current evidence for the involvement of ageing hallmarks in these pathological features of COPD. We also highlight potential novel treatment strategies and opportunities for future research based on our current knowledge of abnormal lung ageing in COPD.
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When compared to aging lungs, there is a significant increase in collagen, fibronectin, and laminin, with more disorganized collagen fibers present in COPD lungs.
“However, when compared to aging lungs, there is a significant increase in collagen, fibronectin, and laminin, with more disorganized collagen fibers present in COPD lungs (139).”
From Aging and Lung Disease (2020) · cites this paper as [139]
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Inflammaging and Oxidative Stress in Human Diseases: From Molecular Mechanisms to Novel Treatments
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Self-citationPulmonary non-tuberculous mycobacterial infections: current state and future management
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COPD-derived fibroblasts secrete higher levels of senescence-associated secretory phenotype proteins
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Self-citationEpithelial cell senescence induces pulmonary fibrosis through Nanog-mediated fibroblast activation
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Role of Molecular Hydrogen in Ageing and Ageing‐Related Diseases
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- Authors
- Brandsma, C.-A., de Vries, M., Costa, R., Woldhuis, R. R., Königshoff, M., & Timens, W.
- Affiliations
- University Medical Center Groningen (NL)
- Helmholtz Munich (DE)
- Corresponding author
- Brandsma, Corry-Anke
- Venue
- European Respiratory Review
- Publisher
- European Respiratory Society (ERS)
- Published
- 2017-12-06
- Volume
- 26
- Issue
- 146
- Pages
- 170073
- ISSN
- 0905-9180 (ISSN-L)
- 1600-0617
- PMC
- PMC9488745
- OpenAlex
- W2772915294
- Cited by
- 221
- References
- 157
- Citations by year
- 2026: 17 · 2025: 25 · 2024: 29 · 2023: 28 · 2022: 32 · 2021: 34 · 2020: 32 · 2019: 17 · 2018: 7
- FWCI
- 12.57
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Licence
- cc-by-nc
- Locations
- European Respiratory Review (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Site cant be reached (submittedVersion, cc-by-nc)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion, other-oa)
- PuSH - Publication Server of Helmholtz Zentrum München (submittedVersion)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Keywords
- lung aging, chronic obstructive pulmonary disease, lung remodeling, small airway disease, emphysema, COPD phenotypes, early-onset COPD
- MeSH terms
- Adolescent, Adult, Age Factors, Aged, Aged, 80 and over, Aging, Animals, Child, Female, Gene Expression Regulation, Humans, Lung, Male, Middle Aged, Phenotype, Prognosis, Regeneration, Risk Factors, Cellular Senescence, Pulmonary Disease, Chronic Obstructive, Young Adult, Airway Remodeling
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