The DOI matches its Crossref record; 117 of the 117 references it cites were found in a registry or an index.
Pathophysiology of hypertension during preeclampsia: linking placental ischemia with endothelial dysfunction
Abstract
Studies over the last decade have provided exciting new insights into potential mechanisms underlying the pathogenesis of preeclampsia. The initiating event in preeclampsia is generally regarded to be placental ischemia/hypoxia, which in turn results in the elaboration of a variety of factors from the placenta that generates profound effects on the cardiovascular system. This host of molecules includes factors such as soluble fms-like tyrosine kinase-1, the angiotensin II type 1 receptor autoantibody, and cytokines such as tumor necrosis factor-α, which generate widespread dysfunction of the maternal vascular endothelium. This dysfunction manifests as enhanced formation of factors such as endothelin, reactive oxygen species, and augmented vascular sensitivity to angiotensin II. Alternatively, the preeclampsia syndrome may also be evidenced as decreased formation of vasodilators such as nitric oxide and prostacyclin. Taken together, these alterations cause hypertension by impairing renal pressure natriuresis and increasing total peripheral resistance. Moreover, the quantitative importance of the various endothelial and humoral factors that mediate vasoconstriction and elevation of arterial pressure during preeclampsia remains to be elucidated. Thus identifying the connection between placental ischemia/hypoxia and maternal cardiovascular abnormalities in hopes of revealing potential therapeutic regimens remains an important area of investigation and will be the focus of this review.
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1 retracted
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RetractedMaynard, S. E., Min, J.-Y., Merchan, J., Lim, K.-H., Li, J., Mondal, S., Libermann, T. A., Morgan, J. P., Sellke, F. W., Stillman, I. E., et al. (2003) · Journal of Clinical Investigation · doi:10.1172/jci17189 · Cited by 4,101
Circulating angiogenic factors and the risk of preeclampsia
Levine, R. J., Maynard, S. E., Qian, C., Lim, K.-H., England, L. J., Yu, K. F., Schisterman, E. F., Thadhani, R., Sachs, B. P., Epstein, F. H., et al. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa031884 · Cited by 3,720
Circulating angiogenic factors and the risk of preeclampsia*
(2004) · Obstetrics & Gynecology · doi:10.1097/00006250-200405000-00028 · Cited by 2,615
Preeclampsia: an endothelial cell disorder
Roberts, J. M., Taylor, R. N., Musci, T. J., Rodgers, G. M., Hubel, C. A., & McLaughlin, M. K. (1989) · American Journal of Obstetrics and Gynecology · doi:10.1016/0002-9378(89)90665-0 · Cited by 1,859
Soluble endoglin contributes to the pathogenesis of preeclampsia
Venkatesha, S., Toporsian, M., Lam, C., Hanai, J.-I., Mammoto, T., Kim, Y. M., Bdolah, Y., Lim, K.-H., Yuan, H.-T., Libermann, T. A., et al. (2006) · Nature Medicine · doi:10.1038/nm1429 · Cited by 1,855
Soluble Endoglin and Other Circulating Antiangiogenic Factors in Preeclampsia
Levine, R. J., Lam, C., Qian, C., Yu, K. F., Maynard, S. E., Sachs, B. P., Sibai, B. M., Epstein, F. H., Romero, R., Thadhani, R., et al. (2006) · New England Journal of Medicine · doi:10.1056/nejmoa055352 · Cited by 1,802
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Soluble Endoglin and Other Circulating Antiangiogenic Factors in Preeclampsia
(2006) · New England Journal of Medicine · doi:10.1056/nejmx060063 · Cited by 1,235
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Cited by
Inflammatory cytokines in vascular dysfunction and vascular disease
Sprague, A. H., & Khalil, R. A. (2009) · Biochemical Pharmacology · doi:10.1016/j.bcp.2009.04.029 · Cited by 1,352
Cardiovascular sequelae of preeclampsia/eclampsia: A systematic review and meta-analyses
McDonald, S. D., Malinowski, A., Zhou, Q., Yusuf, S., & Devereaux, P. J. (2008) · American Heart Journal · doi:10.1016/j.ahj.2008.06.042 · Cited by 924
Kell, D. B. (2009) · BMC Medical Genomics · doi:10.1186/1755-8794-2-2 · Cited by 554
Normal Pregnancy- A State of Insulin Resistance
Sonagra, A. D. (2014) · JOURNAL OF CLINICAL AND DIAGNOSTIC RESEARCH · doi:10.7860/jcdr/2014/10068.5081 · Cited by 268
Hypertension: Physiology and Pathophysiology
Hall, J. E., Granger, J. P., do Carmo, J. M., da Silva, A. A., Dubinion, J., George, E., Hamza, S., Speed, J., & Hall, M. E. (2012) · Comprehensive Physiology · doi:10.1002/cphy.c110058 · Cited by 232
Self-citation
Metadata
- Authors
- Gilbert, J. S., Ryan, M. J., LaMarca, B. B., Sedeek, M., Murphy, S. R., & Granger, J. P.
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2008-02
- Volume
- 294
- Issue
- 2
- Pages
- H541-H550
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W2132961242
- Cited by
- 558
- References
- 117
- FWCI
- 34.63
- Type
- journal article
- Language
- en
- Open access
- closed
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- Gilbert, J. S., Ryan, M. J., LaMarca, B. B., Sedeek, M., Murphy, S. R., & Granger, J. P. (2008). Pathophysiology of hypertension during preeclampsia: linking placental ischemia with endothelial dysfunction. American Journal of Physiology-Heart and Circulatory Physiology. https://doi.org/10.1152/ajpheart.01113.2007
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