Evidence map›Paper›PMID 19337544›Full record

ReviewVascular health and risk management2008

Pathophysiology of placentation abnormalities in pregnancy-induced hypertension.

Mitsuko Furuya, Junji Ishida, Ichiro Aoki, Akiyoshi Fukamizu

Open access · goldAbstract readReview
In one paragraph

Review in Vascular health and risk management, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 90 citations in OpenAlex.

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  17. Role of the NLRP3 Inflammasome in Preeclampsia.Frontiers in endocrinology · 2020
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  20. Observational
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 1 institution in 1 country.

Mitsuko FuruyaDepartment of Pathology, Yokohama City University Graduate School of Medicine, 3-9 Fuku-ura, Kanazawa, Yokohama, Japan. mfuruya@yokohama-cu.ac.jp
Junji Ishida
Ichiro Aoki
Akiyoshi Fukamizu
Yokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During embryogenesis and development, the fetus obtains oxygen and nutrients from the mother through placental microcirculation. The placenta is a distinctive organ that develops and differentiates per se, and that organizes fetal growth and maternal condition in the entire course of gestation. Several life-threatening diseases during pregnancy, such as pregnancy-induced hypertension (PIH) and eclampsia, are closely associated with placental dysfunction. Genetic susceptibilities and poor placentation have been investigated intensively to understand the pathophysiology of PIH. It is currently thought that "poor placentation hypothesis", in which extravillous trophoblasts fail to invade sufficiently the placental bed, explains in part maternal predisposition to this disease. Cumulative studies have suggested that hypoxic micromilieu of fetoplacental site, shear stress of uteroplacental blood flow, and aberrantly secreted proinflammatory substances into maternal circulation synergistically contribute to the progression of PIH. For example, soluble form of vascular endothelial growth factor receptor-1 (sVEGFR-1) and soluble form of CD105 are elevated in circulation of PIH mothers. However, it remains to be poorly understood the pathological events in the placenta during the last half of gestation as maternal systemic disorders get worse. For better understanding and effective therapeutic approaches to PIH, it is important to clarify pathological course of PIH-associated changes in the placenta. In this review, current understanding of placental development and the pathophysiology of PIH placenta are summarized. In addition, recent findings of vasoactive signalings in PIH and rodent PIH models are discussed.

Indexed as

Placental CirculationPlacentationAnimalsAntihypertensive AgentsCell DifferentiationDisease Models, AnimalEmbryo ImplantationEndothelial CellsFemaleFetal Growth RetardationGestational AgeHumansHypertension, Pregnancy-InducedInflammationInflammation MediatorsNeovascularization, PhysiologicAntihypertensive AgentsInflammation MediatorsReceptor, Angiotensin, Type 1intrauterine growth restrictionneovascularizationplacentapreeclampsiapregnancy-induced hypertensionrenin –angiotensin-systemtransgenic mice

Identifiers

PMID19337544
PMCPMC2663465
OpenAlexW1643693347

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.