Evidence map›Paper›PMID 33042016›Full record

ReviewFrontiers in endocrinology2020

Mechanisms of Endothelial Dysfunction in Pre-eclampsia and Gestational Diabetes Mellitus: Windows Into Future Cardiometabolic Health?

Colm J McElwain, Eszter Tuboly, Fergus P McCarthy, Cathal M McCarthy

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed, 1 pooled it
7.5field-weighted citation impact, top 2% 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

114 citing papers in PubMed, 1 synthesis or guideline pooled it, 180 citations in OpenAlex.

  1. Pooled it
  2. Article
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  5. Overlap of Gestational Diabetes Mellitus and Pre-eclampsia: A Scoping Review.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2026
    Review
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54 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

4 authors at 2 institutions in 1 country.

Colm J McElwainDepartment of Pharmacology and Therapeutics, Western Gateway Building, University College Cork, Cork, Ireland.
Eszter TubolyDepartment of Pharmacology and Therapeutics, Western Gateway Building, University College Cork, Cork, Ireland.
Fergus P McCarthyDepartment of Obstetrics and Gynaecology, Cork University Maternity Hospital, Cork, Ireland.
Cathal M McCarthyDepartment of Pharmacology and Therapeutics, Western Gateway Building, University College Cork, Cork, Ireland.
University College Cork · IECork University Hospital · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Placental insufficiency and adipose tissue dysregulation are postulated to play key roles in the pathophysiology of both pre-eclampsia (PE) and gestational diabetes mellitus (GDM). A dysfunctional release of deleterious signaling motifs can offset an increase in circulating oxidative stressors, pro-inflammatory factors and various cytokines. It has been previously postulated that endothelial dysfunction, instigated by signaling from endocrine organs such as the placenta and adipose tissue, may be a key mediator of the vasculopathy that is evident in both adverse obstetric complications. These signaling pathways also have significant effects on long term maternal cardiometabolic health outcomes, specifically cardiovascular disease, hypertension, and type II diabetes. Recent studies have noted that both PE and GDM are strongly associated with lower maternal flow-mediated dilation, however the exact pathways which link endothelial dysfunction to clinical outcomes in these complications remains in question. The current diagnostic regimen for both PE and GDM lacks specificity and consistency in relation to clinical guidelines. Furthermore, current therapeutic options rely largely on clinical symptom control such as antihypertensives and insulin therapy, rather than that of early intervention or prophylaxis. A better understanding of the pathogenic origin of these obstetric complications will allow for more targeted therapeutic interventions. In this review we will explore the complex signaling relationship between the placenta and adipose tissue in PE and GDM and investigate how these intricate pathways affect maternal endothelial function and, hence, play a role in acute pathophysiology and the development of future chronic maternal health outcomes.

Indexed as

Adipose TissueAnimalsCardiometabolic Risk FactorsCardiovascular DiseasesDiabetes, GestationalEndothelial CellsFemaleHumansInsulin ResistancePlacentaPre-EclampsiaPregnancySignal Transductionadiposityendothelial dysfunctionGDMmitochondriaoxidative stressPEtherapeutics

Identifiers

PMID33042016
PMCPMC7516342
OpenAlexW3086407586

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.