The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Role of apoptosis in the pathogenesis of COPD and pulmonary emphysema
Open accessAbstract
Chronic obstructive pulmonary disease (COPD) is characterised by chronic inflammation of the airways and progressive destruction of lung parenchyma, a process that in most cases is initiated by cigarette smoking. Several mechanisms are involved in the development of the disease: influx of inflammatory cells into the lung (leading to chronic inflammation of the airways), imbalance between proteolytic and anti-proteolytic activity (resulting in the destruction of healthy lung tissue) and oxidative stress. Recently, an increasing number of data suggest a fourth important mechanism involved in the development of COPD: apoptosis of structural cells in the lung might possibly be an important upstream event in the pathogenesis of COPD. There is an increase in apoptotic alveolar epithelial and endothelial cells in the lungs of COPD patients. Since this is not counterbalanced by an increase in proliferation of these structural cells, the net result is destruction of lung tissue and the development of emphysema. Data from animal models suggest a role for Vascular Endothelial Growth Factor (VEGF) in the induction of apoptosis of structural cells in the lung. Other mediators of apoptosis, such as caspase-3 and ceramide, could be interesting targets to prevent apoptosis and the development of emphysema. In this review, recent data on the role of apoptosis in COPD from both animal models as well as from studies on human subjects will be discussed. The aim is to provide an up to date summary on the increasing knowledge on the role of apoptosis in COPD and pulmonary emphysema.
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Two CD95 (APO‐1/Fas) signaling pathways
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“Others have suggested that humoral- and CD4+ celldependent mechanisms can lead to alveolar septal cell apoptosis and the development of emphysema [51].”
BackgroundSkeletal Muscle Apoptosis and Weight Loss in Chronic Obstructive Pulmonary Disease
Agustí, A. G. N., Sauleda, J., Miralles, C., Gomez, C., Togores, B., Sala, E., Batle, S., & Busquets, X. (2002) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.2108013 · Cited by 343
Cited by
Activated PMN Exosomes: Pathogenic Entities Causing Matrix Destruction and Disease in the Lung
Genschmer, K. R., Russell, D. W., Lal, C., Szul, T., Bratcher, P. E., Noerager, B. D., Abdul Roda, M., Xu, X., Rezonzew, G., Viera, L., et al. (2019) · Cell · doi:10.1016/j.cell.2018.12.002 · Cited by 445
Garcia-Arcos, I., Geraghty, P., Baumlin, N., Campos, M., Dabo, A. J., Jundi, B., Cummins, N., Eden, E., Grosche, A., Salathe, M., et al. (2016) · Thorax · doi:10.1136/thoraxjnl-2015-208039 · Cited by 339
Pathogenic triad in COPD: oxidative stress, protease–antiprotease imbalance, and inflammation
Fischer, B., Pavlisko, E., & Voynow, J. (2011) · International Journal of Chronic Obstructive Pulmonary Disease · doi:10.2147/copd.s10770 · Cited by 301
Lung ageing and COPD: is there a role for ageing in abnormal tissue repair?
Brandsma, C.-A., de Vries, M., Costa, R., Woldhuis, R. R., Königshoff, M., & Timens, W. (2017) · European Respiratory Review · doi:10.1183/16000617.0073-2017 · Cited by 221
Cigarette Smoke Particle-Induced Lung Injury and Iron Homeostasis
Ghio, A. J., Pavlisko, E. N., Roggli, V. L., Todd, N. W., & Sangani, R. G. (2022) · International Journal of Chronic Obstructive Pulmonary Disease · doi:10.2147/copd.s337354 · Cited by 19
Metadata
- Authors
- Demedts, I. K., Demoor, T., Bracke, K. R., Joos, G. F., & Brusselle, G. G.
- Venue
- Respiratory Research
- Published
- 2006-03-30
- Volume
- 7
- Issue
- 1
- Pages
- 53-53
- ISSN
- 1465-9921 (ISSN-L)
- 1465-993X
- OpenAlex
- W1870141733
- Cited by
- 541
- References
- 5
- FWCI
- 15.56
- Type
- journal article
- Language
- en
- Open access
- gold
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- Demedts, I. K., Demoor, T., Bracke, K. R., Joos, G. F., & Brusselle, G. G. (2006). Role of apoptosis in the pathogenesis of COPD and pulmonary emphysema. Respiratory Research. https://doi.org/10.1186/1465-9921-7-53
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
