Evidence map›Paper›PMID 36777173›Full record

ArticleJACC. Basic to translational science2023

Tie2-Cre-Induced Inactivation of Non-Nuclear Estrogen Receptor-α Signaling Abrogates Estrogen Protection Against Vascular Injury.

Pang-Yen Liu, Nobuaki Fukuma, Yukio Hiroi, Akiko Kunita, Hiroyuki Tokiwa, Kazutaka Ueda, Taro Kariya, Genri Numata, Yusuke Adachi, Miyu Tajima and 10 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JACC. Basic to translational science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 27% 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

4 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
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

20 authors at 7 institutions in 3 countries.

Pang-Yen LiuDivision of Cardiology, Department of Internal Medicine, Tri-Service General Hospital Penghu Branch, National Defense Medical Center, Taipei, Taiwan.
Nobuaki FukumaDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yukio HiroiNational Center for Global Health and Medicine, Tokyo, Japan.
Akiko KunitaDepartment of Pathology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Hiroyuki TokiwaDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kazutaka UedaDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Taro KariyaDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Genri NumataDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yusuke AdachiDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Miyu TajimaDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Masayuki ToyodaDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yuxin LiVascular Medicine Research, Brigham and Women's Hospital and Harvard Medical School, Cambridge, Massachusetts, USA.
Kensuke NomaVascular Medicine Research, Brigham and Women's Hospital and Harvard Medical School, Cambridge, Massachusetts, USA.
Mutsuo HaradaDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Haruhiro TokoDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Tetsuo UshikuDepartment of Pathology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Yoshimitsu KanaiDepartment of Anatomy and Cell Biology, Wakayama Medical University, School of Medicine, Wakayama, Japan.
Eiki TakimotoDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
James K LiaoVascular Medicine Research, Brigham and Women's Hospital and Harvard Medical School, Cambridge, Massachusetts, USA.
Issei KomuroDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
The University of Tokyo · JPBrigham and Women's Hospital · USHiroshima University · JPJohns Hopkins University · USNihon University · JPTri-Service General Hospital · TWWakayama Medical University · JP

Funding

Mechanisms Underlying Vascular AgingR01HL136962 · NHLBI · UNIVERSITY OF CHICAGO · PI LIAO, JAMES KUANG-JAN · 2018 to 2021
$1.8M
NHLBI NIH HHS R01 HL136962
6 · The paper itself

Abstract

Using the Cre-loxP system, we generated the first mouse model in which estrogen receptor-α non-nuclear signaling was inactivated in endothelial cells. Estrogen protection against mechanical vascular injury was impaired in this model. This result indicates the pivotal role of endothelial estrogen receptor-α non-nuclear signaling in the vasculoprotective effects of estrogen.

Indexed as

cDNA, complementary deoxyribonucleic acidE2, 17β-estradiolECGM, endothelial cell growth mediumendothelial cellseNOS, endothelial nitric oxide synthaseER, estrogen receptorERαKI/KI, estrogen receptor-αknock-in/knock-inestrogen receptor-αLVEDD, left ventricular end-diastolic diameternon-nuclear signalingNOS, nitric oxide synthasePI3K, phosphatidylinositol 3-kinasePLA, proximity ligation assaytissue-specific regulationVo2, oxygen consumption

Identifiers

PMID36777173
PMCPMC9911321
OpenAlexW4309144636

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.