Evidence map›Paper›PMID 30659198›Full record

ArticleScientific reports2019

Tadalafil treatment in mice for preeclampsia with fetal growth restriction has neuro-benefic effects in offspring through modulating prenatal hypoxic conditions.

Ryota Tachibana, Takashi Umekawa, Kento Yoshikawa, Takao Owa, Shoichi Magawa, Fumi Furuhashi, Makoto Tsuji, Shintaro Maki, Kyoko Shimada, Michiko K Kaneda and 14 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.2field-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

21 citing papers in PubMed, 38 citations in OpenAlex.

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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

24 authors at 5 institutions in 1 country.

Ryota TachibanaDepartment of Obstetrics and Gynecology, Mie University Graduate School of Medicine, Tsu, Japan.
Takashi UmekawaDepartment of Obstetrics and Gynecology, Mie University Graduate School of Medicine, Tsu, Japan.
Kento YoshikawaDepartment of Obstetrics and Gynecology, Mie University Graduate School of Medicine, Tsu, Japan.
Takao OwaDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, Osaka, Japan.
Shoichi MagawaDepartment of Obstetrics and Gynecology, Mie University Graduate School of Medicine, Tsu, Japan.
Fumi FuruhashiDepartment of Obstetrics and Gynecology, Mie University Graduate School of Medicine, Tsu, Japan.
Makoto TsujiDepartment of Obstetrics and Gynecology, Mie University Graduate School of Medicine, Tsu, Japan.
Shintaro MakiDepartment of Obstetrics and Gynecology, Mie University Graduate School of Medicine, Tsu, Japan.
Kyoko ShimadaDepartment of Obstetrics and Gynecology, Mie University Graduate School of Medicine, Tsu, Japan.
Michiko K KanedaDepartment of Obstetrics and Gynecology, Mie University Graduate School of Medicine, Tsu, Japan.
Masafumi NiiDepartment of Obstetrics and Gynecology, Mie University Graduate School of Medicine, Tsu, Japan.
Hiroaki TanakaDepartment of Obstetrics and Gynecology, Mie University Graduate School of Medicine, Tsu, Japan. hakumei.s52@gmail.com.
Kayo TanakaDepartment of Obstetrics and Gynecology, Mie University Graduate School of Medicine, Tsu, Japan.
Yuki KamimotoDepartment of Obstetrics and Gynecology, Mie University Graduate School of Medicine, Tsu, Japan.
Eiji KondoDepartment of Obstetrics and Gynecology, Mie University Graduate School of Medicine, Tsu, Japan.
Ineko KatoDepartment of Obstetrics and Gynecology, Mie University Graduate School of Medicine, Tsu, Japan.
Kenji IkemuraDepartment of Pharmacy, Mie University Hospital, Tsu, Japan.ORCID 0000-0003-1870-9571
Masahiro OkudaDepartment of Pharmacy, Mie University Hospital, Tsu, Japan.
Ning MaFaculty of Health Science, Suzuka University of Medical Science, Suzuka, Japan.
Takekazu MiyoshiDepartment of Perinatology and Gynecology, National Cerebral and Cardiovascular Center, Suita, Japan.ORCID 0000-0003-0834-2411
Hiroshi HosodaDepartment of Regenerative Medicine and Tissue Engineering, National Cerebral and Cardiovascular Center, Suita, Japan.
Masayuki EndohDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, Osaka, Japan.
Tadashi KimuraDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, Osaka, Japan.
Tomoaki IkedaDepartment of Obstetrics and Gynecology, Mie University Graduate School of Medicine, Tsu, Japan.
Mie University · JPThe University of Osaka · JPMie University Hospital · JPNational Cerebral and Cardiovascular Center · JPSuzuka University of Medical Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have demonstrated that tadalafil facilitates fetal growth in mice with L-NG-nitroarginine methyl ester (L-NAME)-induced preeclampsia (PE) with fetal growth restriction (FGR). Tadalafil is a selective phosphodiesterase 5 inhibitor that dilates the maternal blood sinuses in the placenta, thereby facilitating the growth of the fetus. The purpose of this study was to investigate the effects of tadalafil treatment for PE and FGR on the developing brain in FGR offspring using an L-NAME-induced mouse model of PE with FGR. A control group of dams received carboxymethylcellulose (CMC). L-NAME-treated groups received L-NAME dissolved in CMC from 11 days post coitum (d.p.c.). The L-NAME-treated dams were divided into two subgroups 14 d.p.c. One subgroup continued to receive L-NAME. The other subgroup received L-NAME with tadalafil suspended in CMC. Tadalafil treatment for PE with FGR reduced the expression of hypoxia-inducible factor-2α in the placenta and in the brain of the FGR fetus. Moreover, tadalafil treatment in utero shows improved synaptogenesis and myelination in FGR offspring on postnatal day 15 (P15) and P30. These results suggest that tadalafil treatment for PE with FGR not only facilitates fetal growth, but also has neuroprotective effects on the developing brain of FGR offspring through modulating prenatal hypoxic conditions.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsBrainDisease Models, AnimalEndothelial PAS Domain-Containing Protein 1FemaleFetal Growth RetardationHypoxiaMicePlacentaPre-EclampsiaPregnancyTadalafilTreatment OutcomeVasodilator AgentsBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1TadalafilVasodilator Agents

Identifiers

PMID30659198
PMCPMC6338749
OpenAlexW2908591663

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.