Evidence map›Paper›PMID 23321791›Full record

ArticleAutophagy2013

Impaired autophagy by soluble endoglin, under physiological hypoxia in early pregnant period, is involved in poor placentation in preeclampsia.

Akitoshi Nakashima, Mikiko Yamanaka-Tatematsu, Naonobu Fujita, Keiichi Koizumi, Tomoko Shima, Toshiko Yoshida, Toshio Nikaido, Aikou Okamoto, Tamotsu Yoshimori, Shigeru Saito

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
9.3field-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

104 citing papers in PubMed, 219 citations in OpenAlex.

  1. Trial
  2. An Integrated Proteomics and Genomics Approach to Identify Essential Protein Kinases During Human Trophoblast Development.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
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  4. Hyperadhesive von Willebrand Factor Contributes to Pathogenesis of Preeclampsia.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
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44 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

10 authors at 3 institutions in 1 country.

Akitoshi NakashimaDepartment of Obstetrics and Gynecology, Faculty of Medicine, University of Toyama, Toyama, Japan.
Mikiko Yamanaka-Tatematsu
Naonobu Fujita
Keiichi Koizumi
Tomoko Shima
Toshiko Yoshida
Toshio Nikaido
Aikou Okamoto
Tamotsu Yoshimori
Shigeru Saito
University of Toyama · JPOsaka University · JPJikei University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In early pregnancy, trophoblasts and the fetus experience hypoxic and low-nutrient conditions; nevertheless, trophoblasts invade the uterine myometrium up to one third of its depth and migrate along the lumina of spiral arterioles, replacing the maternal endothelial lining. Here, we showed that autophagy, an intracellular bulk degradation system, occurred in extravillous trophoblast (EVT) cells under hypoxia in vitro and in vivo. An enhancement of autophagy was observed in EVTs in early placental tissues, which suffer from physiological hypoxia. The invasion and vascular remodeling under hypoxia were significantly reduced in autophagy-deficient EVT cells compared with wild-type EVT cells. Interestingly, soluble endoglin (sENG), which increased in sera in preeclamptic cases, suppressed EVT invasion by inhibiting autophagy. The sENG-inhibited EVT invasion was recovered by TGFB1 treatment in a dose-dependent manner. A high dose of sENG inhibited the vascular construction by EVT cells and human umbilical vein endothelial cells (HUVECs), meanwhile a low dose of sENG inhibited the replacement of HUVECs by EVT cells. A protein selectively degraded by autophagy, SQSTM1, accumulated in EVT cells in preeclamptic placental biopsy samples showing impaired autophagy. This is the first report showing that impaired autophagy in EVT contributes to the pathophysiology of preeclampsia.

Indexed as

AutophagyAdaptor Proteins, Signal TransducingAdultAntigens, CDCell HypoxiaCell LineCell ProliferationEndoglinFemaleGreen Fluorescent ProteinsHumansHuman Umbilical Vein Endothelial CellsOxygenPlacentaPre-EclampsiaPregnancyAdaptor Proteins, Signal TransducingAntigens, CDEndoglinENG protein, humanGreen Fluorescent ProteinsOxygenReceptors, Cell SurfaceRecombinant ProteinsSequestosome-1 ProteinSQSTM1 protein, humanautophagyextravillous trophoblasthypoxiainvasionpreeclampsiasoluble endoglinSQSTM1

Identifiers

PMID23321791
PMCPMC3590252
OpenAlexW2077675917

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.