Evidence map›Paper›PMID 27903516›Full record

SynthesisAmerican journal of physiology. Regulatory, integrative and comparative physiology2017

Metabolic abnormalities and obesity's impact on the risk for developing preeclampsia.

Frank T Spradley

Open access · bronzeAbstract readMeta-AnalysisReview
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in American journal of physiology. Regulatory, integrative and comparative physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 4% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.

  1. Pooled it
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  11. Pathophysiology of Maternal Obesity and Hypertension in Pregnancy.Journal of cardiovascular development and disease · 2025
    Review
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2 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

1 author at 1 institution in 1 country.

Frank T SpradleyDepartment of Surgery, Department of Physiology and Biophysics, Cardiovascular-Renal Research Center, Women's Health Research Center, The University of Mississippi Medical Center, Jackson, Mississippi fspradley@umc.edu.
University of Mississippi Medical Center · US

Funding

The role of leptin in autoimmune-associated hypertensionP20GM104357 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI ALEXANDER, BARBARA T · 2013 to 2022
$23.4M
Effect of obesity on antiangiogenic and inflammatory mechanisms mediating hypertension during pregnancyK99HL130577 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI SPRADLEY, FRANK TRAVIS · 2016 to 2016
$89k
NHLBI NIH HHS K99 HL130577NIGMS NIH HHS P20 GM104357
6 · The paper itself

Abstract

Preeclampsia (PE), a hypertensive disorder of pregnancy, is increasing as a major contributor to perinatal and long-term morbidity of mother and offspring. PE is thought to originate from ischemic insults in the placenta driving the release of prohypertensive anti-angiogenic [soluble fms-like tyrosine kinase-1 (sFlt-1)] and proinflammatory [tumor necrosis factor-α (TNF-α)] factors into the maternal circulation. Whereas the increased incidence of PE is hypothesized to be largely due to the obesity pandemic, the mechanisms whereby obesity increases this risk are unknown. The maternal endothelium is targeted by placental and adipose tissue-derived factors like sFlt-1 and TNF-α that promote hypertension during pregnancy, resulting in vascular dysfunction and hypertension. Interestingly, not all obese pregnant women develop PE. Data suggest that obese pregnant women with the greatest metabolic abnormalities have the highest incidence of PE. Identifying obesity-related mechanisms driving hypertension in some obese pregnant women and pathways that protect normotensive obese pregnant women, may uncover novel protocols to treat PE. Metabolic abnormalities, such as increased circulating leptin, glucose, insulin, and lipids, are likely to increase the risk for PE in obese women. It is not only important to understand whether each of these metabolic factors contribute to the increased risk for PE in obesity, but also their cumulative effects. This is particularly relevant to obese pregnant women with gestational diabetes mellitus (GDM) where all of these factors are increased and the risk for PE is highest. It is speculated that these factors potentiate the anti-angiogenic and proinflammatory mechanisms of placental ischemia-induced vascular dysfunction thereby contributing to the increasing incidence of PE.

Indexed as

BiomarkersCausalityComorbidityCytokinesEvidence-Based MedicineFemaleHumansImmunologic FactorsMetabolic DiseasesObesityPre-EclampsiaPregnancyRisk FactorsBiomarkersCytokinesImmunologic Factorsadipose tissueendotheliumgestational diabetes mellitushypertensionwomen’s health

Identifiers

PMID27903516
PMCPMC5283940
OpenAlexW2557445216

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.