Evidence map›Paper›PMID 24327973›Full record

ReviewObstetrics & gynecology science2013

Pathogenesis and promising non-invasive markers for preeclampsia.

Young Ju Kim

Open access · diamondAbstract readReview
In one paragraph

Review in Obstetrics & gynecology science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 9% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Article
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  4. Hypoxic modulation of fetal vascular MLCK abundance, localization, and function.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
    Article
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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.

Young Ju KimDepartment of Obstetrics and Gynecology, Ewha Womans University School of Medicine, Seoul, Korea.
Ewha Womans University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Preeclampsia is one of the leading causes of maternal mortality/morbidity and preterm delivery in the world, affecting 3% to 5% of pregnant women. The pathophysiology of preeclampsia likely involves both maternal and fetal/placental factors. Abnormalities in the development of placental vessels early in pregnancy may result in placental hypoperfusion, hypoxia, or ischemia. Hypoperfusion, hypoxia, and ischemia are critical components in the pathogenesis of preeclampsia because the hypoperfused placenta transfers many factors into maternal vessels that alter maternal endothelial cell function and lead to the systemic symptoms of preeclampsia. There are several hypotheses to explain the pathogenesis of preeclampsia, including altered angiogenic balance, circulating angiogenic factors (such as marinobufagenin, a bufadienolide trigger), and activation of the renin-angiotensin system. Epigenetically-modified cell-free nucleic acids that circulate in plasma and serum might be novel markers with promising non-invasive clinical applications in the diagnosis of preeclampsia.

Indexed as

Angiogenic factorsCell-free nucleic acidsMarinobufageninPathogenesisPreeclampsia

Identifiers

PMID24327973
PMCPMC3784103
OpenAlexW2044362396

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.