Vascular biology of preeclampsia
Open accessAbstract
Preeclampsia, a pregnancy-specific syndrome characterized by hypertension, proteinuria and edema, resolves on delivery of the placenta. Normal pregnancy is itself characterized by systemic inflammation, oxidative stress and alterations in levels of angiogenic factors and vascular reactivity. This is exacerbated in preeclampsia with an associated breakdown of compensatory mechanisms, eventually leading to placental and vascular dysfunction. The underlying pathology of preeclampsia is thought to be a relatively hypoxic or ischemic placenta. Both the placenta and maternal vasculatures are major sources of reactive oxygen and nitrogen species which can interact to produce peroxynitrite a powerful prooxidant that covalently modifies proteins by nitration of tyrosine residues, to possibly alter vascular function in preeclampsia. The linkage between placental hypoxia and maternal vascular dysfunction has been proposed to be via placental syncytiotrophoblast basement membranes shed by the placenta or via angiogenic factors which include soluble flt1 and endoglin secreted by the placenta that bind vascular endothelial growth factor (VEGF) and placental growth factor (PIGF) in the maternal circulation. There is also abundant evidence of altered reactivity of the maternal and placental vasculature and of the altered production of autocoids in preeclampsia. The occurrence of preeclampsia is increased in women with preexisting vascular disease and confers a long-term risk for development of cardiovascular disease. The vascular stress test of pregnancy thus identifies those women with a previously unrecognized at risk vascular system and promotes the development of preeclampsia. Preexisting maternal vascular dysfunction intensified by placental factors is possibly responsible for the individual pathologies of preeclampsia.
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Gui et al. suggested that metformin reduced the rate of gestational hypertension because of its effects on endothelial function and its decrease in the production of reactive oxygen species.
“Gui et al.(75) suggested that metformin reduced the rate of gestational hypertension because of its effects on endothelial function and its decrease in the production of reactive oxygen species, the two mechanisms implicated in the pathophysiology of preeclampsia(84–94).”
From Metformin, the Aspirin of the 21st Century: Its Role in Gestational Diabetes Mellitus, Prevention of Preeclampsia and Cancer, and the Promotion of Longevity (2017) · cites this paper as [86]
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Self-citationProtein Nitration in Placenta – Functional Significance
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Self-citationThe Clinical Significance of Hemodilution during Pregnancy
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Decrease and Senescence of Endothelial Progenitor Cells in Patients with Preeclampsia
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Increased Nitrotyrosine in the Diabetic Placenta: Evidence for oxidative stress
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Self-citationNitric oxide for preventing pre-eclampsia and its complications
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Self-citationDoes a predisposition to the metabolic syndrome sensitize women to develop pre-eclampsia?
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Study of Plasma Factors Associated With Neutrophil Activation and Lipid Peroxidation in Preeclampsia
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Placenta growth factor is not an early marker for the development of severe preeclampsia
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Being born small for gestational age increases the risk of severe pre‐eclampsia
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Risk for Coronary Artery Disease and Morbid Preeclampsia: A Commentary
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Current Paradigms in Cellular Oxygen Sensing
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Romero, R., Erez, O., Hüttemann, M., Maymon, E., Panaitescu, B., Conde-Agudelo, A., Pacora, P., Yoon, B. H., & Grossman, L. I. (2017) · American Journal of Obstetrics and Gynecology · doi:10.1016/j.ajog.2017.06.003 · Cited by 253 · see citing works
Clark, A. R., James, J. L., Stevenson, G. N., & Collins, S. L. (2018) · Placenta · doi:10.1016/j.placenta.2018.05.001 · Cited by 86 · see citing works
Szalai, G., Romero, R., Chaiworapongsa, T., Xu, Y., Wang, B., Ahn, H., Xu, Z., Chiang, P. J., Sundell, B., Wang, R., et al. (2015) · PLoS ONE · doi:10.1371/journal.pone.0119547 · Cited by 46 · see citing works
- Authors
- Myatt, L., & Webster, R. P.
- Affiliations
- University of Cincinnati (US)
- Corresponding author
- Webster, R.P.
- ORCID
- Myatt, L.
- Venue
- Journal of Thrombosis and Haemostasis
- Publisher
- Elsevier BV
- Published
- 2009-03
- Volume
- 7
- Issue
- 3
- Pages
- 375-384
- ISSN
- 1538-7836 (ISSN-L)
- OpenAlex
- W2040119916
- Cited by
- 292
- References
- 153
- Citations by year
- 2026: 6 · 2025: 9 · 2024: 19 · 2023: 14 · 2022: 16 · 2021: 16 · 2020: 13 · 2019: 18 · 2018: 13 · 2017: 16 · 2016: 16 · 2015: 27 · 2014: 25 · 2013: 17 · 2012: 22
- FWCI
- 2.25
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of Thrombosis and Haemostasis (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Health Sciences › Medicine › Psychiatry and Mental health › Neurological Complications and Syndromes
- Life Sciences › Immunology and Microbiology › Immunology › Reproductive System and Pregnancy
- Keywords
- preeclampsia, placental hypoxia, placental ischemia, peroxynitrite, reactive oxygen species, reactive nitrogen species, CD105, vascular endothelial growth factor, placental growth factor, angiogenic factors, vascular dysfunction, maternal hypertension, proteinuria, cardiovascular risk, oxidative stress, systemic inflammation
- MeSH terms
- Blood Vessels, Endothelium, Vascular, Female, Humans, Placenta, Pre-Eclampsia, Pregnancy
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