The DOI matches its Crossref record; 18 of the 18 references it cites were found in a registry or an index.
The Endothelial Biology of Sickle Cell Disease: Inflammation and a Chronic Vasculopathy
Abstract
A single amino acid substitution in hemoglobin comprises the molecular basis for sickle cell anemia, but evolution of the corresponding clinical disease is extraordinarily complicated and likely involves multiple pathogenic factors. Sickle disease is fundamentally an inflammatory state, with activation of the endothelium, probably through proximate effects of reperfusion injury physiology and chronic molestation by adherent red cells and white cells. The disease also involves enhanced angiogenic propensity, activation of coagulation, disordered vasoregulation, and a component of chronic vasculopathy. Sickle cell anemia is truly an endothelial disease, and it is likely that genetic differences in endothelial function help govern its astonishing phenotypic diversity.
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Cites
Inflammation in atherosclerosis
Libby, P. (2002) · Nature · doi:10.1038/nature01323 · Cited by 8,315
Acute-Phase Proteins and Other Systemic Responses to Inflammation
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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
Mortality in sickle cell disease. Life expectancy and risk factors for early death
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“It is interesting, given that female humans with sickle disease have greater bioavailability of NO (58) and longevity (139) compared to males, that female rodents were selectively protected due to action of hepatic eNOS in a nonsickle model of liver ischemia– reperfusion (69).”
BackgroundLandmesser, U., Dikalov, S., Price, S. R., McCann, L., Fukai, T., Holland, S. M., Mitch, W. E., & Harrison, D. G. (2003) · Journal of Clinical Investigation · doi:10.1172/jci200314172 · Cited by 1,660
Cell-free hemoglobin limits nitric oxide bioavailability in sickle-cell disease
Reiter, C. D., Wang, X., Tanus-Santos, J. E., Hogg, N., Cannon, R. O., Schechter, A. N., & Gladwin, M. T. (2002) · Nature Medicine · doi:10.1038/nm1202-799 · Cited by 1,330
Causes and Outcomes of the Acute Chest Syndrome in Sickle Cell Disease
Vichinsky, E. P., Neumayr, L. D., Earles, A. N., Williams, R., Lennette, E. T., Dean, D., Nickerson, B., Orringer, E., McKie, V., Bellevue, R., et al. (2000) · New England Journal of Medicine · doi:10.1056/nejm200006223422502 · Cited by 1,234
Sulfasalazine: A potent and specific inhibitor of nuclear factor kappa B
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Prediction of Adverse Outcomes in Children with Sickle Cell Disease
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“Also, leukocytosis predicts which babies will subsequently develop a severe clinical course (123).”
BackgroundStroke in a cohort of patients with homozygous sickle cell disease
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Cited by
Thrombosis in paroxysmal nocturnal hemoglobinuria
Hill, A., Kelly, R. J., & Hillmen, P. (2013) · Blood · doi:10.1182/blood-2012-09-311381 · Cited by 478
Villagra, J., Shiva, S., Hunter, L. A., Machado, R. F., Gladwin, M. T., & Kato, G. J. (2007) · Blood · doi:10.1182/blood-2006-12-061697 · Cited by 384
Kato, G. J., Hebbel, R. P., Steinberg, M. H., & Gladwin, M. T. (2009) · American Journal of Hematology · doi:10.1002/ajh.21475 · Cited by 349
Self-citationSickle Red Cell–Endothelium Interactions
KAUL, D. K., FINNEGAN, E., & BARABINO, G. A. (2009) · Microcirculation · doi:10.1080/10739680802279394 · Cited by 208
Self-citationMaitra, P., Caughey, M., Robinson, L., Desai, P. C., Jones, S., Nouraie, M., Gladwin, M. T., Hinderliter, A., Cai, J., & Ataga, K. I. (2017) · Haematologica · doi:10.3324/haematol.2016.153791 · Cited by 137
Metadata
- Authors
- HEBBEL, R. P., OSAROGIAGBON, R., & KAUL, D.
- Venue
- Microcirculation
- Publisher
- Wiley
- Published
- 2004-03
- Volume
- 11
- Issue
- 2
- Pages
- 129-151
- ISSN
- 1073-9688 (ISSN-L)
- 1549-8719
- OpenAlex
- W2155803841
- Cited by
- 463
- References
- 18
- FWCI
- 8.48
- 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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