Evidence map›Paper›PMID 25810297›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2015

Endothelial glucocorticoid receptor suppresses atherogenesis--brief report.

Julie E Goodwin, Xinbo Zhang, Noemi Rotllan, Yan Feng, Han Zhou, Carlos Fernández-Hernando, Jun Yu, William C Sessa

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

22 citing papers in PubMed, 31 citations in OpenAlex.

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  5. Loss of endothelial glucocorticoid receptor accelerates organ fibrosis inAmerican journal of physiology. Renal physiology · 2023
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  6. Review
  7. Loss of endothelial glucocorticoid receptor accelerates organ fibrosis inbioRxiv : the preprint server for biology · 2023
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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

8 authors at 1 institution in 1 country.

Julie E Goodwin *Department of Pediatrics, Yale University School of Medicine, New Haven, CT.
Xinbo ZhangVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT.
Noemi RotllanIntegrative Cell Signaling and Neurobiology of Metabolism Program, Section of Comparative Medicine, Yale University School of Medicine, New Haven, CT.
Yan FengDepartment of Pediatrics, Yale University School of Medicine, New Haven, CT.
Han ZhouDepartment of Pediatrics, Yale University School of Medicine, New Haven, CT.
Carlos Fernández-HernandoIntegrative Cell Signaling and Neurobiology of Metabolism Program, Section of Comparative Medicine, Yale University School of Medicine, New Haven, CT.
Jun YuVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT.
William C SessaVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT.
Cardiovascular Research Center · BR

Funding

PHOSPHORYLATION AND ENDOTHELIAL NITRIC OXIDE PRODUCTIONR01HL064793 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2000 to 2016
$6.3M
Endothelial NOS by protein to protein interactionsR37HL061371 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2009 to 2017
$4.1M
Regulation of vascular remodeling &angiogenesis by NogoR01HL081190 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2005 to 2014
$4.1M
Endothelial NOS by Protein-Protein IntractionsR01HL061371 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 1999 to 2008
$3.6M
Role of RTN-4 in AtherosclerosisR56HL117064 · NHLBI · YALE UNIVERSITY · PI YU, JUN · 2013 to 2013
$416k
NHLBI NIH HHS HL081190NHLBI NIH HHS HL117064NHLBI NIH HHS HL61371NHLBI NIH HHS HL64793NHLBI NIH HHS R01 HL061371NHLBI NIH HHS R01 HL064793NHLBI NIH HHS R01 HL081190NHLBI NIH HHS R37 HL061371NHLBI NIH HHS R56 HL117064
6 · The paper itself

Abstract

objectiveThe purpose of this study was to determine the role of the endothelial glucocorticoid receptor in the pathogenesis of atherosclerosis. APPROACH AND

resultsControl mice and mice lacking the endothelial glucocorticoid receptor were bred onto an Apoe knockout background and subjected to high-fat diet feeding for 12 weeks. Assessment of body weight and total cholesterol and triglycerides before and after the diet revealed no differences between the 2 groups of mice. However, mice lacking the endothelial glucocorticoid receptor developed more severe atherosclerotic lesions in the aorta, brachiocephalic artery, and aortic sinus, as well as a heightened inflammatory milieu as evidenced by increased macrophage recruitment in the lesions.

conclusionsThese data suggest that the endothelial glucocorticoid receptor is important for tonic inhibition of inflammation and limitation of atherosclerosis progression in this model.

Indexed as

AnimalsAortaAortic DiseasesApolipoproteins EAtherosclerosisBody WeightBrachiocephalic TrunkCholesterolDiet, High-FatDisease Models, AnimalEndothelial CellsGenotypeMacrophagesMice, Inbred C57BLMice, KnockoutPhenotypeApolipoproteins ECholesterolNR3C1 protein, mouseReceptors, GlucocorticoidTriglyceridesatherosclerosisendotheliumglucocorticoid receptor

Identifiers

PMID25810297
PMCPMC4375730
OpenAlexW2105000051

What OpenQuestion holds

Textmetadata
LicenceTDM
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.