The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Hypoxia-Induced Pulmonary Vascular Remodeling: Cellular and Molecular Mechanisms
Abstract
Chronic hypoxic exposure induces changes in the structure of pulmonary arteries, as well as in the biochemical and functional phenotypes of each of the vascular cell types, from the hilum of the lung to the most peripheral vessels in the alveolar wall. The magnitude and the specific profile of the changes depend on the species, sex, and the developmental stage at which the exposure to hypoxia occurred. Further, hypoxia-induced changes are site specific, such that the remodeling process in the large vessels differs from that in the smallest vessels. The cellular and molecular mechanisms vary and depend on the cellular composition of vessels at particular sites along the longitudinal axis of the pulmonary vasculature, as well as on local environmental factors. Each of the resident vascular cell types (ie, endothelial, smooth muscle, adventitial fibroblast) undergo site- and time-dependent alterations in proliferation, matrix protein production, expression of growth factors, cytokines, and receptors, and each resident cell type plays a specific role in the overall remodeling response. In addition, hypoxic exposure induces an inflammatory response within the vessel wall, and the recruited circulating progenitor cells contribute significantly to the structural remodeling and persistent vasoconstriction of the pulmonary circulation. The possibility exists that the lung or lung vessels also contain resident progenitor cells that participate in the remodeling process. Thus the hypoxia-induced remodeling of the pulmonary circulation is a highly complex process where numerous interactive events must be taken into account as we search for newer, more effective therapeutic interventions. This review provides perspectives on each of the aforementioned areas.
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Cites
Cellular and developmental control of O 2 homeostasis by hypoxia-inducible factor 1α
Iyer, N. V., Kotch, L. E., Agani, F., Leung, S. W., Laughner, E., Wenger, R. H., Gassmann, M., Gearhart, J. D., Lawler, A. M., Yu, A. Y., et al. (1998) · Genes & Development · doi:10.1101/gad.12.2.149 · Cited by 2,476
Oxygen sensing by HIF hydroxylases
Schofield, C. J., & Ratcliffe, P. J. (2004) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1366 · Cited by 2,068
Ema, M., Taya, S., Yokotani, N., Sogawa, K., Matsuda, Y., & Fujii-Kuriyama, Y. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.9.4273 · Cited by 1,016
Perspective Article: Tissue repair, contraction, and the myofibroblast
Desmoulière, A., Chaponnier, C., & Gabbiani, G. (2005) · Wound Repair and Regeneration · doi:10.1111/j.1067-1927.2005.130102.x · Cited by 892
Moulton, K. S., Vakili, K., Zurakowski, D., Soliman, M., Butterfield, C., Sylvin, E., Lo, K.-M., Gillies, S., Javaherian, K., & Folkman, J. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0730843100 · Cited by 652
Proline hydroxylation and gene expression
Kaelin, W. G. (2005) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.74.082803.133142 · Cited by 468
Elvidge, G. P., Glenny, L., Appelhoff, R. J., Ratcliffe, P. J., Ragoussis, J., & Gleadle, J. M. (2006) · Journal of Biological Chemistry · doi:10.1074/jbc.m511408200 · Cited by 464
The biology of hypoxia: the role of oxygen sensing in development, normal function, and disease
Giaccia, A. J., Simon, M. C., & Johnson, R. (2004) · Genes & Development · doi:10.1101/gad.1243304 · Cited by 380
Schultz, K., Fanburg, B. L., & Beasley, D. (2006) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.01077.2005 · Cited by 159
Pulmonary hypertension and inflammation
Tuder, R. M., & Voelkel, N. F. (1998) · Journal of Laboratory and Clinical Medicine · doi:10.1016/s0022-2143(98)90020-8 · Cited by 128
Cited by
Pathophysiology of Sleep Apnea
Dempsey, J. A., Veasey, S. C., Morgan, B. J., & O'Donnell, C. P. (2010) · Physiological Reviews · doi:10.1152/physrev.00043.2008 · Cited by 2,243
Fibroblasts in fibrosis: novel roles and mediators
Kendall, R. T., & Feghali-Bostwick, C. A. (2014) · Frontiers in Pharmacology · doi:10.3389/fphar.2014.00123 · Cited by 1,082
Stenmark, K. R., Meyrick, B., Galie, N., Mooi, W. J., & McMurtry, I. F. (2009) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00217.2009 · Cited by 774
Self-citationChan, S. Y., Zhang, Y.-Y., Hemann, C., Mahoney, C. E., Zweier, J. L., & Loscalzo, J. (2009) · Cell Metabolism · doi:10.1016/j.cmet.2009.08.015 · Cited by 702
“In particular, this response may be especially important to the pulmonary vascular endothelium, which directly responds to hypoxia by controlling the release of vasoactive effectors, thereby critically influencing normal vascular physiology and the development of pulmonary hypertension (Stenmark et al., 2006).”
Prabhakar, N. R., & Semenza, G. L. (2012) · Physiological Reviews · doi:10.1152/physrev.00030.2011 · Cited by 641
Metadata
- Authors
- Stenmark, K. R., Fagan, K. A., & Frid, M. G.
- Venue
- Circulation Research
- Published
- 2006-09-29
- Volume
- 99
- Issue
- 7
- Pages
- 675-691
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2165946847
- Cited by
- 1,006
- References
- 10
- FWCI
- 27.64
- Type
- journal article
- Language
- en
- Open access
- closed
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