Evidence map›Paper›PMID 27451103›Full record

ArticleAdvances in pharmacology (San Diego, Calif.)2016

Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia.

J S Possomato-Vieira, R A Khalil

Open access · greenAbstract read
In one paragraph

Article in Advances in pharmacology (San Diego, Calif.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed, 2 pooled it
95.5field-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

107 citing papers in PubMed, 2 syntheses or guidelines pooled it, 229 citations in OpenAlex.

  1. Pooled it
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  3. Trial
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  6. Exploring the Mechanism of Postpartum Cognitive Dysfunction in a Preeclampsia Rat Model via Multimodal Imaging.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  7. Article
  8. Therapeutic Interventions for Preeclampsia: Integrating Placental and Maternal Perspectives.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026
    Review
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  18. taVNS alleviates preeclampsia-induced vascular endothelial dysfunction via α7nAChR- IP3R1/GRP75/VDAC1 signal pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  19. Review
  20. Article

47 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 2 institutions in 1 country.

J S Possomato-VieiraVascular Surgery Research Laboratories, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States.
R A KhalilVascular Surgery Research Laboratories, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States. Electronic address: raouf_khalil@hms.harvard.edu.
Brigham and Women's Hospital · USHarvard University · US

Funding

Vascular Mechanisms in Pregnancy-Induced HypertensionR01HL065998 · NHLBI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI KHALIL, RAOUF A · 2002 to 2016
$4.3M
Mechano-Sensitive Hypoxia-Inducible Factor-MMP Pathway in Venous InsufficiencyR21HL111775 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI KHALIL, RAOUF A · 2013 to 2014
$475k
NHLBI NIH HHS R01 HL065998NHLBI NIH HHS R21 HL111775
6 · The paper itself

Abstract

Preeclampsia is a pregnancy-related disorder characterized by hypertension and could lead to maternal and fetal morbidity and mortality. Although the causative factors and pathophysiological mechanisms are unclear, endothelial dysfunction is a major hallmark of preeclampsia. Clinical tests and experimental research have suggested that generalized endotheliosis in the systemic, renal, cerebral, and hepatic circulation could decrease endothelium-derived vasodilators such as nitric oxide, prostacyclin, and hyperpolarization factor and increase vasoconstrictors such as endothelin-1 and thromboxane A2, leading to increased vasoconstriction, hypertension, and other manifestation of preeclampsia. In search for the upstream mechanisms that could cause endothelial dysfunction, certain genetic, demographic, and environmental risk factors have been suggested to cause abnormal expression of uteroplacental integrins, cytokines, and matrix metalloproteinases, leading to decreased maternal tolerance, apoptosis of invasive trophoblast cells, inadequate spiral arteries remodeling, reduced uterine perfusion pressure (RUPP), and placental ischemia/hypoxia. RUPP may cause imbalance between the antiangiogenic factors soluble fms-like tyrosine kinase-1 and soluble endoglin and the proangiogenic factors vascular endothelial growth factor and placental growth factor, or stimulate the release of other circulating bioactive factors such as inflammatory cytokines, hypoxia-inducible factor-1, reactive oxygen species, and angiotensin AT1 receptor agonistic autoantibodies. These circulating factors could then target endothelial cells and cause generalized endothelial dysfunction. Therapeutic options are currently limited, but understanding the factors involved in endothelial dysfunction could help design new approaches for prediction and management of preeclampsia.

Indexed as

AnimalsEndothelium, VascularFemaleHumansHypertension, Pregnancy-InducedHypoxiaIschemiaPlacentaPre-EclampsiaPregnancyReactive Oxygen SpeciesVascular Endothelial Growth Factor AReactive Oxygen SpeciesVascular Endothelial Growth Factor ACytokinesEndothelinEndotheliumGrowth factorsHypertensionHypoxiaNitric oxideOxidative stressPlacental ischemia

Identifiers

PMID27451103
PMCPMC4965238
OpenAlexW2499431560

What OpenQuestion holds

Textmetadata
LicenceTDM
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.