Evidence map›Paper›PMID 30897333›Full record

ArticleAmerican journal of respiratory cell and molecular biology2019

Endothelial-Mesenchymal Transition Drives Expression of CD44 Variant and xCT in Pulmonary Hypertension.

Sarasa Isobe, Masaharu Kataoka, Jin Endo, Hidenori Moriyama, Shogo Okazaki, Kenji Tsuchihashi, Yoshinori Katsumata, Tsunehisa Yamamoto, Kohsuke Shirakawa, Naohiro Yoshida and 8 more

Abstract read
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In one paragraph

Article in American journal of respiratory cell and molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed, 35 citations in OpenAlex.

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  10. Role of histone lactylation interference RNA mFrontiers in cell and developmental biology · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 6 institutions in 2 countries.

Sarasa IsobeDepartment of Cardiology.
Masaharu KataokaDepartment of Cardiology.
Jin EndoDepartment of Cardiology.
Hidenori MoriyamaDepartment of Cardiology.
Shogo OkazakiDivision of Gene Regulation, Institute for Advanced Medical Research.
Kenji TsuchihashiDivision of Gene Regulation, Institute for Advanced Medical Research.
Yoshinori KatsumataDepartment of Cardiology.
Tsunehisa YamamotoDepartment of Cardiology.
Kohsuke ShirakawaDepartment of Cardiology.
Naohiro YoshidaDepartment of Cardiology.
Masayuki ShimodaDepartment of Pathology, and.
Tomohiro ChibaDepartment of Pathology, Kyorin University School of Medicine, Tokyo, Japan.
Takashi MasukoDepartment of Pharmaceutical Sciences, Cell Biology Laboratory, Faculty of Pharmacy, Kindai University, Osaka, Japan; and.
Yoji HakamataDepartment of Basic Science, School of Veterinary Nursing and Technology, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, Tokyo, Japan.
Eiji KobayashiDepartment of Organ Fabrication, Keio University School of Medicine, Tokyo, Japan.
Hideyuki SayaDivision of Gene Regulation, Institute for Advanced Medical Research.
Keiichi FukudaDepartment of Cardiology.
Motoaki SanoDepartment of Cardiology.
Institute for Advanced Medical Research · USKeio University · JPKindai University · JPKyorin University · JPNippon Veterinary and Life Science University · JPTokyo Women's Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) pathogenesis shares similarities with carcinogenesis. One CD44 variant (CD44v) isoform, CD44v8-10, binds to and stabilizes the cystine transporter subunit (xCT), producing reduced glutathione and thereby enhancing the antioxidant defense of cancer stem cells. Pharmacological inhibition of xCT by sulfasalazine suppresses tumor growth, survival, and resistance to chemotherapy. We investigated whether the CD44v-xCT axis contributes to PAH pathogenesis. CD44v was predominantly expressed on endothelial-to-mesenchymal transition (EndMT)-like cells in the neointimal layer of PAH affected pulmonary arterioles.

Indexed as

AnimalsCell ProliferationEndothelial CellsGlutathioneHyaluronan ReceptorsHypertension, PulmonaryMiceNeoplastic Stem CellsProtein IsoformsReactive Oxygen SpeciesSulfasalazineCd44 protein, mouseGlutathioneHyaluronan ReceptorsProtein IsoformsReactive Oxygen SpeciesSulfasalazineCD44 variant isoformendothelial–mesenchymal transitionpulmonary arterial hypertensionsulfasalazinexCT

Identifiers

PMID30897333
OpenAlexW2923547474

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.