Evidence map›Paper›PMID 33670947›Full record

ReviewInternational journal of molecular sciences2021

Aggrephagy Deficiency in the Placenta: A New Pathogenesis of Preeclampsia.

Akitoshi Nakashima, Tomoko Shima, Sayaka Tsuda, Aiko Aoki, Mihoko Kawaguchi, Atsushi Furuta, Ippei Yasuda, Satoshi Yoneda, Akemi Yamaki-Ushijima, Shi-Bin Cheng and 2 more

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

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  14. Deeply in Plasticenta: Presence of Microplastics in the Intracellular Compartment of Human Placentas.International journal of environmental research and public health · 2022
    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

12 authors at 2 institutions in 2 countries.

Akitoshi NakashimaDepartment of Obstetrics and Gynecology, University of Toyama, Toyama 9300194, Japan.
Tomoko ShimaDepartment of Obstetrics and Gynecology, University of Toyama, Toyama 9300194, Japan.
Sayaka TsudaDepartment of Obstetrics and Gynecology, University of Toyama, Toyama 9300194, Japan.
Aiko AokiDepartment of Obstetrics and Gynecology, University of Toyama, Toyama 9300194, Japan.
Mihoko KawaguchiDepartment of Obstetrics and Gynecology, University of Toyama, Toyama 9300194, Japan.
Atsushi FurutaDepartment of Obstetrics and Gynecology, University of Toyama, Toyama 9300194, Japan.
Ippei YasudaDepartment of Obstetrics and Gynecology, University of Toyama, Toyama 9300194, Japan.
Satoshi YonedaDepartment of Obstetrics and Gynecology, University of Toyama, Toyama 9300194, Japan.
Akemi Yamaki-UshijimaDepartment of Obstetrics and Gynecology, University of Toyama, Toyama 9300194, Japan.
Shi-Bin ChengDepartment of Pediatrics, Women and Infants Hospital of Rhode Island, Warren Alpert Medical School of Brown University, Providence, RI 02905, USA.
Surendra SharmaDepartment of Pediatrics, Women and Infants Hospital of Rhode Island, Warren Alpert Medical School of Brown University, Providence, RI 02905, USA.
Shigeru SaitoUniversity of Toyama, Toyama 9308555, Japan.ORCID 0000-0002-8940-3708
University of Toyama · JPBrown University · US

Funding

JSPS KAKENHI 20K09614JSPS KAKENHI JP19K09750NIH HHS P20GM121298-05
6 · The paper itself

Abstract

Aggrephagy is defined as the selective degradation of aggregated proteins by autophagosomes. Protein aggregation in organs and cells has been highlighted as a cause of multiple diseases, including neurodegenerative diseases, cardiac failure, and renal failure. Aggregates could pose a hazard for cell survival. Cells exhibit three main mechanisms against the accumulation of aggregates: protein refolding by upregulation of chaperones, reduction of protein overload by translational inhibition, and protein degradation by the ubiquitin-proteasome and autophagy-lysosome systems. Deletion of autophagy-related genes reportedly contributes to intracellular protein aggregation in vivo. Some proteins recognized in aggregates in preeclamptic placentas include those involved in neurodegenerative diseases. As aggregates are derived both intracellularly and extracellularly, special endocytosis for extracellular aggregates also employs the autophagy machinery. In this review, we discuss how the deficiency of aggrephagy and/or macroautophagy leads to poor placentation, resulting in preeclampsia or fetal growth restriction.

Indexed as

MacroautophagyAnimalsFemaleHumansLysosomesPlacentaPre-EclampsiaPregnancyProtein Aggregation, Pathologicalaggrephagyaggresomeautophagyendoplasmic reticulum stressinflammationplacentapreeclampsiapregnancyprotein aggregationtransthyretin

Identifiers

PMID33670947
PMCPMC7957664
OpenAlexW3135073994

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.