The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Cellular and Connective Tissue Changes in Alveolar Septal Walls in Emphysema
Abstract
Emphysema is commonly defined as enlargement of airspaces distal to terminal bronchioles accompanied by destruction of alveolar walls, but without obvious fibrosis. Morphometric techniques were used to correlate changes in components of the alveolar septa surrounding enlarged airspaces in human emphysema with the mean linear intercept (Lm) of those airspaces. Alveolar and capillary surface density decreased with increased Lm, but the ratio of these surface densities to each other remained close to normal for mild to moderate increases in Lm. This suggests that the decreased gas exchange observed in emphysema is initiated by a total loss of septa and not by selective pathological changes of the microvasculature. Increases in septal wall thickness directly correlated with increases in Lm. For the mild to moderate emphysema lesions included in this study, an increase of 100% in Lm correlated with a 130% increase in the relative volume of the alveolar septal interstitium. Significant increases occurred in both elastin (0.14 to 0.56 microm(3)/microm(2) basement membrane [BM]) and collagen (0.49 to 1. 63 microm(3)/microm(2) BM). The increase in elastin and collagen raises the possibility of a remodeling process in the connective matrix in alveolar walls. Whether or not the new connective tissue represents a disordered, nonfunctional regional response needs to be determined.
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Hubbard, R. C., Ogushi, F., Fells, G. A., Cantin, A. M., Jallat, S., Courtney, M., & Crystal, R. G. (1987) · Journal of Clinical Investigation · doi:10.1172/jci113204 · Cited by 157 · cited 1×
“It is believed that macrophages play a role in the pathogenesis of the alveolar septal injury that characterizes pulmonary emphysema, and that they may be important especially in the pathogenesis of chronic tissue destruction (10, 29 ).”
Background
Cited by
Cellular and Structural Bases of Chronic Obstructive Pulmonary Disease
SAETTA, M., TURATO, G., MAESTRELLI, P., MAPP, C. E., & FABBRI, L. M. (2001) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/ajrccm.163.6.2009116 · Cited by 552
Burgstaller, G., Oehrle, B., Gerckens, M., White, E. S., Schiller, H. B., & Eickelberg, O. (2017) · European Respiratory Journal · doi:10.1183/13993003.01805-2016 · Cited by 482
The role of integrins in inflammation and angiogenesis
Mezu-Ndubuisi, O. J., & Maheshwari, A. (2021) · Pediatric Research · doi:10.1038/s41390-020-01177-9 · Cited by 384
Remodeling and Inflammation of Bronchi in Asthma and Chronic Obstructive Pulmonary Disease
Jeffery, P. K. (2004) · Proceedings of the American Thoracic Society · doi:10.1513/pats.200402-009ms · Cited by 347
Extracellular matrix in lung development, homeostasis and disease
Zhou, Y., Horowitz, J. C., Naba, A., Ambalavanan, N., Atabai, K., Balestrini, J., Bitterman, P. B., Corley, R. A., Ding, B.-S., Engler, A. J., et al. (2018) · Matrix Biology · doi:10.1016/j.matbio.2018.03.005 · Cited by 284
Metadata
- Authors
- VLAHOVIC, G., RUSSELL, M. L., MERCER, R. R., & CRAPO, J. D.
- Venue
- American Journal of Respiratory and Critical Care Medicine
- Publisher
- Oxford University Press (OUP)
- Published
- 1999-12-01
- Volume
- 160
- Issue
- 6
- Pages
- 2086-2092
- ISSN
- 1073-449X (ISSN-L)
- 1535-4970
- OpenAlex
- W2119946727
- Cited by
- 195
- References
- 1
- FWCI
- 3.26
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: Cellular and Connective Tissue Changes in Alveolar Septal Walls in Emphysema. https://app.cochat.ai/papers/10.1164/ajrccm.160.6.9706031
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- VLAHOVIC, G., RUSSELL, M. L., MERCER, R. R., & CRAPO, J. D. (1999). Cellular and Connective Tissue Changes in Alveolar Septal Walls in Emphysema. American Journal of Respiratory and Critical Care Medicine. https://doi.org/10.1164/ajrccm.160.6.9706031
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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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