Evidence map›Paper›PMID 23590594›Full record

ReviewActa physiologica (Oxford, England)2013

Pathophysiology of hypertension in pre-eclampsia: a lesson in integrative physiology.

A C Palei, F T Spradley, J P Warrington, E M George, J P Granger

Open access · greenAbstract readReview
In one paragraph

Review in Acta physiologica (Oxford, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed, 4 pooled it
14.9field-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

106 citing papers in PubMed, 4 syntheses or guidelines pooled it, 224 citations in OpenAlex.

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  12. Interleukin-1 receptor type 1 inhibition improves blood pressure, fetal growth and immune balance in placental ischemic rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2025
    Article
  13. Article
  14. The Role of Angiogenetic Factors in Preeclampsia.International journal of molecular sciences · 2025
    Review
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  18. Evaluating oxidative stress targeting treatments inFrontiers in cell and developmental biology · 2025
    Article
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46 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

5 authors at 2 institutions in 1 country.

A C PaleiDepartment of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, USA.
F T Spradley
J P Warrington
E M George
J P Granger
University of Mississippi Medical Center · USJackson Memorial Hospital · US

Funding

STRUCTURAL VASCULAR ADAPTATION OF THE MICROCIRCULATIONP01HL051971 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI HESTER, ROBERT L · 1993 to 2018
$39.4M
Hypertension and Cardiorenal Research Training ProgramT32HL105324 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI Joey P. Granger · 2010 to 2026
$7.8M
Hypertension, Kidney and PregnancyR01HL108618 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI GRANGER, JOEY P. · 2011 to 2015
$1.8M
NHLBI NIH HHS 1T32HL105324NHLBI NIH HHS HL051971NHLBI NIH HHS HL108618NHLBI NIH HHS P01 HL051971NHLBI NIH HHS R01 HL108618NHLBI NIH HHS T32 HL105324
6 · The paper itself

Abstract

Despite being one of the leading causes of maternal death and a major contributor of maternal and perinatal morbidity, the mechanisms responsible for the pathogenesis of pre-eclampsia have yet to be fully elucidated. However, it is evident that this is a complex disorder involving multiple organ systems, and by using integrative approaches, enormous progress has been made towards understanding the pathophysiology of pre-eclampsia. Growing evidence supports the concept that the placenta plays a central role in the pathogenesis of pre-eclampsia and that reduced uteroplacental perfusion, which develops as a result of abnormal cytotrophoblast invasion of spiral arterioles, triggers the cascade of events leading to the maternal disorder. Placental ischaemia leads to release of soluble placental factors, many of which are classified as anti-angiogenic or pro-inflammatory. Once these ischaemic placental factors reach the maternal circulation, they cause widespread activation and dysfunction of the maternal vascular endothelium that results in enhanced formation of endothelin-1 and superoxide, increased vascular sensitivity to angiotensin II and decreased formation of vasodilators such as nitric oxide. This review highlights these links between placental ischaemia, maternal endothelial activation and renal dysfunction in the pathogenesis of hypertension in pre-eclampsia.

Indexed as

FemaleHumansHypertension, Pregnancy-InducedPlacentaPre-EclampsiaPregnancy

Identifiers

PMID23590594
PMCPMC3687012
OpenAlexW1964249453

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.