Evidence map›Paper›PMID 32762557›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2020

Vascular mechanisms and molecular targets in hypertensive pregnancy and preeclampsia.

Hongmei Qu, Raouf A Khalil

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 2 pooled it
10.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

96 citing papers in PubMed, 2 syntheses or guidelines pooled it, 195 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Hypertension Management in Pregnancy and Postpartum.Journal of the American Society of Nephrology : JASN · 2026
    Review
  6. Article
  7. Observational
  8. Long non-coding RNA maternally expressed gene 3 (Turkish journal of obstetrics and gynecology · 2026
    Article
  9. Article
  10. Observational
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

36 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Hongmei QuVascular Surgery Research Laboratories, Division of Vascular and Endovascular Surgery, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts.
Raouf A KhalilVascular Surgery Research Laboratories, Division of Vascular and Endovascular Surgery, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts.
Brigham and Women's Hospital · US

Funding

Vascular Mechanisms of Hypertension-in-PregnancyR56HL147889 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI KHALIL, RAOUF A · 2019 to 2019
$647k
HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI) R56HL147889-01NHLBI NIH HHS R56 HL147889
6 · The paper itself

Abstract

Preeclampsia is a major complication of pregnancy manifested as hypertension and often intrauterine growth restriction, but the underlying pathophysiological mechanisms are unclear. Predisposing genetic and environmental factors cause placental maladaptations leading to defective placentation, apoptosis of invasive cytotrophoblasts, inadequate expansive remodeling of the spiral arteries, reduced uteroplacental perfusion pressure, and placental ischemia. Placental ischemia promotes the release of bioactive factors into the maternal circulation, causing an imbalance between antiangiogenic soluble fms-like tyrosine kinase-1 and soluble endoglin and proangiogenic vascular endothelial growth factor, placental growth factor, and transforming growth factor-β. Placental ischemia also stimulates the release of proinflammatory cytokines, hypoxia-inducible factor, reactive oxygen species, and angiotensin type 1 receptor agonistic autoantibodies. These circulating factors target the vascular endothelium, causing generalized endotheliosis in systemic, renal, cerebral, and hepatic vessels, leading to decreases in endothelium-derived vasodilators such as nitric oxide, prostacyclin, and hyperpolarization factor and increases in vasoconstrictors such as endothelin-1 and thromboxane A

Indexed as

Arterial PressureAnimalsFemaleHumansHypertension, Pregnancy-InducedHypoxiaIschemiaPlacentaPlacentationPre-EclampsiaPregnancyRisk FactorsSignal TransductionUterine ArteryVascular RemodelingVascular Stiffnesscytokinesendotheliumhypertensionplacental ischemiavascular smooth muscle

Identifiers

PMID32762557
PMCPMC7509272
OpenAlexW3048084405

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.