ReviewComprehensive Physiology2024
Maternal Microvascular Dysfunction During and After Preeclamptic Pregnancy.
Review in Comprehensive Physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed.
- Pravastatin Corrects Endothelial Dysfunction in Ex Vivo Uterine Radial Arteries in Preeclampsia.Acta physiologica (Oxford, England) · 2026Trial
- Oral Losartan Treatment Improves Microvascular Endothelial Function via Nitric Oxide-Dependent Mechanisms in Women With a History of Preeclampsia.American journal of hypertension · 2025Trial
- The Immuno-Cardiovascular Storm of Pre-Eclampsia: Cytokine-Mediated Endothelial Injury, Thrombosis, and Maternal Cardiovascular Instability.Comprehensive Physiology · 2026Review
- Pregnancy- the ultimate cardiovascular stress test.NPJ cardiovascular health · 2026Review
- Visionary AI: Decoding Systemic Vascular Health and Hypertensive Disorders in Pregnancy Through Retinal Imaging and Artificial Intelligence.medRxiv : the preprint server for health sciences · 2025Article
- Closer look at the cardiovascular and metabolic predictors of postpartum depression.World journal of psychiatry · 2025Article
- Reductions in angiotensin II type 2 receptor-mediated vasodilation contribute to increased angiotensin II vasoconstrictor sensitivity in women with preeclampsia history.Clinical science (London, England : 1979) · 2025Article
- Reduced ATHypertension (Dallas, Tex. : 1979) · 2025Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Preeclampsia, a pregnancy disorder characterized by de novo hypertension and maternal multisystem organ dysfunction, is the leading cause of maternal mortality worldwide and is associated with a fourfold greater risk of cardiovascular disease throughout the lifespan. Current understanding of the etiology of preeclampsia remains unclear, due in part to the varying phenotypical presentations of the disease, which has hindered the development of effective and mechanism-specific treatment or prevention strategies both during and after the affected pregnancy. These maternal sequelae of preeclampsia are symptoms of systemic vascular dysfunction in the maternal nonreproductive microvascular beds that drives the development and progression of adverse cardiovascular outcomes during preeclampsia. Despite normalization of vascular disturbances after delivery, subclinical dysfunction persists in the nonreproductive microvascular beds, contributing to an increased lifetime risk of cardiovascular and metabolic diseases and all-cause mortality. Given that women with a history of preeclampsia demonstrate vascular dysfunction despite an absence of traditional CVD risk factors, an understanding of the underlying mechanisms of microvascular dysfunction during and after preeclampsia is essential to identify potential therapeutic avenues to mitigate or reverse the development of overt disease. This article aims to provide a summary of the existing literature on the pathophysiology of maternal microvascular dysfunction during preeclampsia, the mechanisms underlying the residual dysfunction that remains after delivery, and current and potential treatments both during and after the affected pregnancy that may reduce microvascular dysfunction in these high-risk women. © 2024 American Physiological Society. Compr Physiol 14:5703-5727, 2024.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.