The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Expression of angiogenesis‐related molecules in plexiform lesions in severe pulmonary hypertension: evidence for a process of disordered angiogenesis
Abstract
Pulmonary arteries of patients with severe pulmonary hypertension (SPH) presenting in an idiopathic form (primary PH‐PPH) or associated with congenital heart malformations or collagen vascular diseases show plexiform lesions. It is postulated that in lungs with SPH, endothelial cells in plexiform lesions express genes encoding for proteins involved in angiogenesis, in particular, vascular endothelial growth factor (VEGF) and those involved in VEGF receptor‐2 (VEGFR‐2) signalling. On immunohistochemistry and in situ hybridization, endothelial cells in the plexiform lesions expressed VEGF mRNA and protein and overexpressed the mRNA and protein of VEGFR‐2, and the transcription factor subunits HIF‐1α and HIF‐1β of hypoxia inducible factor, which are responsible for the hypoxia‐dependent induction of VEGF. When compared with normal lungs, SPH lungs showed decreased expression of the kinases PI3 kinase and src, which, together with Akt, relay the signal transduction downstream of VEGFR‐2. Because markers of angiogenesis are expressed in plexiform lesions in SPH, it is proposed that these lesions may form by a process of disordered angiogenesis. Copyright © 2001 John Wiley & Sons, Ltd.
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Cites
Vascular endothelial growth factor induced by hypoxia may mediate hypoxia-initiated angiogenesis
Shweiki, D., Itin, A., Soffer, D., & Keshet, E. (1992) · Nature · doi:10.1038/359843a0 · Cited by 4,617
Activation of vascular endothelial growth factor gene transcription by hypoxia-inducible factor 1
Forsythe, J. A., Jiang, B.-H., Iyer, N. V., Agani, F., Leung, S. W., Koos, R. D., & Semenza, G. L. (1996) · Molecular and Cellular Biology · doi:10.1128/mcb.16.9.4604 · Cited by 3,981
Self-citationCellular 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
Self-citationRegulation of Mammalian O 2 Homeostasis by Hypoxia-Inducible Factor 1
Semenza, G. L. (1999) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev.cellbio.15.1.551 · Cited by 1,914 · cited 2×
“Alternatively, HIF-1a expression occurs in endothelial cells that are stimulated to proliferate by growth factors, or as a consequence of genetic mutations [38,40,41].”
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Cited by
Inflammation and immunity in the pathogenesis of pulmonary arterial hypertension
Rabinovitch, M., Guignabert, C., Humbert, M., & Nicolls, M. R. (2014) · Circulation Research · doi:10.1161/circresaha.113.301141 · Cited by 1,029
Mechanisms of disease: pulmonary arterial hypertension
Schermuly, R. T., Ghofrani, H. A., Wilkins, M. R., & Grimminger, F. (2011) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2011.87 · Cited by 800
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
Endothelial Dysfunction in Pulmonary Hypertension
Budhiraja, R., Tuder, R. M., & Hassoun, P. M. (2004) · Circulation · doi:10.1161/01.cir.0000102381.57477.50 · Cited by 768
Self-citationInflammation, Growth Factors, and Pulmonary Vascular Remodeling
Hassoun, P. M., Mouthon, L., Barberà, J. A., Eddahibi, S., Flores, S. C., Grimminger, F., Jones, P. L., Maitland, M. L., Michelakis, E. D., Morrell, N. W., et al. (2009) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2009.04.006 · Cited by 710
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Metadata
- Authors
- Tuder, R. M., Chacon, M., Alger, L., Wang, J., Taraseviciene‐Stewart, L., Kasahara, Y., Cool, C. D., Bishop, A. E., Geraci, M., Semenza, G. L., Yacoub, M., Polak, J. M., & Voelkel, N. F.
- Venue
- The Journal of Pathology
- Publisher
- Wiley
- Published
- 2001-08-29
- Volume
- 195
- Issue
- 3
- Pages
- 367-374
- ISSN
- 0022-3417 (ISSN-L)
- 1096-9896
- OpenAlex
- W2043826113
- Cited by
- 500
- References
- 4
- FWCI
- 10.20
- Type
- journal article
- Language
- en
- Open access
- closed
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