The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Mechanisms of cigarette smoke-induced COPD: insights from animal models
Abstract
Cigarette smoke-induced animal models of chronic obstructive pulmonary disease support the protease-antiprotease hypothesis of emphysema, although which cells and proteases are the crucial actors remains controversial. Inhibition of either serine or metalloproteases produces significant protection against emphysema, but inhibition is invariably accompanied by decreases in the inflammatory response to cigarette smoke, suggesting that these inhibitors do more than just prevent matrix degradation. Direct anti-inflammatory interventions are also effective against the development of emphysema, as are antioxidant strategies; the latter again decrease smoke-induced inflammation. There is increasing evidence for autoimmunity, perhaps directed against matrix components, as a driving force in emphysema. There is intriguing but controversial animal model evidence that failure to repair/failure of lung maintenance also plays a role in the pathogenesis of emphysema. Cigarette smoke produces small airway remodeling in laboratory animals, possibly by direct induction of fibrogenic growth factors in the airway wall, and also produces pulmonary hypertension, at least in part through direct upregulation of vasoactive mediators in the intrapulmonary arteries. Smoke exposure causes goblet cell metaplasia and excess mucus production in the small airways and proximal trachea, but these changes are not good models of either chronic bronchitis or acute exacerbations. Emphysema, small airway remodeling, pulmonary hypertension, and mucus production appear to be at least partially independent processes that may require different therapeutic approaches.
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Cites
Vestbo, J., Hurd, S. S., Agustí, A. G., Jones, P. W., Vogelmeier, C., Anzueto, A., Barnes, P. J., Fabbri, L. M., Martinez, F. J., Nishimura, M., et al. (2013) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.201204-0596pp · Cited by 15,983
Rabe, K. F., Hurd, S., Anzueto, A., Barnes, P. J., Buist, S. A., Calverley, P., Fukuchi, Y., Jenkins, C., Rodriguez-Roisin, R., van Weel, C., et al. (2007) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.200703-456so · Cited by 4,925
Matrix metalloproteinases as modulators of inflammation and innate immunity
Parks, W. C., Wilson, C. L., & López-Boado, Y. S. (2004) · Nature Reviews Immunology · doi:10.1038/nri1418 · Cited by 1,929
Gilmore, A. P. (2005) · Cell Death & Differentiation · doi:10.1038/sj.cdd.4401723 · Cited by 597
Alveolar Cell Senescence in Patients with Pulmonary Emphysema
Tsuji, T., Aoshiba, K., & Nagai, A. (2006) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.200509-1374oc · Cited by 527
Grumelli, S., Corry, D. B., Song, L.-Z., Song, L., Green, L., Huh, J., Hacken, J., Espada, R., Bag, R., Lewis, D. E., et al. (2004) · PLoS Medicine · doi:10.1371/journal.pmed.0010008 · Cited by 484 · cited 2×
“This has stemmed in part from the recognition that a number of metalloproteases, including MMP-9 and MMP-12 (124), can degrade elastin; in part from reports of increased levels of MMPs including MMP-1, -2, -9, -14 (50, 72, 120, 150), and in some studies, MMP-12 (42, 60, 72, 111, 182), in BAL fluid, alveolar macrophage…”
Hurst, J. R., Perera, W. R., Wilkinson, T. M. A., Donaldson, G. C., & Wedzicha, J. A. (2006) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.200505-704oc · Cited by 346
Cigarette smoke induces cellular senescence
Nyunoya, T., Monick, M. M., Klingelhutz, A., Yarovinsky, T. O., Cagley, J. R., & Hunninghake, G. W. (2006) · American Journal of Respiratory Cell and Molecular Biology · doi:10.1165/rcmb.2006-0169oc · Cited by 306
Cited by
Raza, H., John, A., & Nemmar, A. (2013) · Cellular Physiology and Biochemistry · doi:10.1159/000350087 · Cited by 47,221
What are the respiratory effects of e-cigarettes?
Gotts, J. E., Jordt, S.-E., McConnell, R., & Tarran, R. (2019) · BMJ · doi:10.1136/bmj.l5275 · Cited by 516
Animal models of chronic obstructive pulmonary disease
Wright, J. L., Cosio, M., & Churg, A. (2008) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.90200.2008 · Cited by 447
Self-citationVanoirbeek, J. A. J., Rinaldi, M., De Vooght, V., Haenen, S., Bobic, S., Gayan-Ramirez, G., Hoet, P. H. M., Verbeken, E., Decramer, M., Nemery, B., et al. (2010) · American Journal of Respiratory Cell and Molecular Biology · doi:10.1165/rcmb.2008-0487oc · Cited by 320
Talukder, M. A. H., Johnson, W. M., Varadharaj, S., Lian, J., Kearns, P. N., El-Mahdy, M. A., Liu, X., & Zweier, J. L. (2011) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00868.2010 · Cited by 287
Metadata
- Authors
- Churg, A., Cosio, M., & Wright, J. L.
- Venue
- American Journal of Physiology-Lung Cellular and Molecular Physiology
- Publisher
- American Physiological Society
- Published
- 2008-04
- Volume
- 294
- Issue
- 4
- Pages
- L612-L631
- ISSN
- 1040-0605 (ISSN-L)
- 1522-1504
- OpenAlex
- W2144613920
- Cited by
- 319
- References
- 8
- FWCI
- 17.53
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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