Evidence map›Paper›PMID 39256246›Full record

ArticlePflugers Archiv : European journal of physiology2025

Salt-sensitive hypertension in GR mutant rats is associated with altered plasma polyunsaturated fatty acid levels and aortic vascular reactivity.

S Verouti, G Aeschlimann, Q Wang, D Ancin Del Olmo, A C Peyter, S Menétrey, D V Winter, A Odermatt, D Pearce, E Hummler and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

11 authors.

S VeroutiDepartment of Biomedical Sciences, University of Lausanne, Lausanne, Switzerland.ORCID 0000-0002-2297-2738
G AeschlimannDepartment of Biomedical Sciences, University of Lausanne, Lausanne, Switzerland.ORCID 0009-0008-4518-9405
Q WangDivision of Nephrology and Hypertension, Lausanne University Hospital (CHUV), Lausanne, Switzerland.ORCID 0009-0003-8960-4598
D Ancin Del OlmoDepartment of Biomedical Sciences, University of Lausanne, Lausanne, Switzerland.ORCID 0009-0002-6796-3410
A C PeyterNeonatal Research Laboratory, Clinic of Neonatology, Department Woman-Mother-Child, Lausanne University Hospital (CHUV) and University of Lausanne, Lausanne, Switzerland.ORCID 0000-0003-2051-1126
S MenétreyNeonatal Research Laboratory, Clinic of Neonatology, Department Woman-Mother-Child, Lausanne University Hospital (CHUV) and University of Lausanne, Lausanne, Switzerland.ORCID 0000-0002-5831-4534
D V WinterDivision of Molecular and Systems Toxicology, Department of Pharmaceutical Sciences, University of Basel, Basel, Switzerland.ORCID 0000-0002-3764-1747
A OdermattDivision of Molecular and Systems Toxicology, Department of Pharmaceutical Sciences, University of Basel, Basel, Switzerland.ORCID 0000-0002-6820-2712
D PearceDepartment of Medicine and Cellular & Molecular Pharmacology, University of California, San Francisco, USA.ORCID 0000-0003-0496-3173
E HummlerDepartment of Biomedical Sciences, University of Lausanne, Lausanne, Switzerland.ORCID 0000-0002-3887-2715
P E VanderrieleDepartment of Biomedical Sciences, University of Lausanne, Lausanne, Switzerland. Paulemmanuelvanderriele@gmail.com.ORCID 0000-0002-8581-8471

Funding

National Center of Competence in Research N-403-07-23Swiss National Science Foundation grants 310030-214978Swiss National Science Foundation grants 31003A-182478/1
6 · The paper itself

Abstract

In humans, glucocorticoid resistance is attributed to mutations in the glucocorticoid receptor (GR). Most of these mutations result in decreased ligand binding, transactivation, and/or translocation, albeit with normal protein abundances. However, there is no clear genotype‒phenotype relationship between the severity or age at disease presentation and the degree of functional loss of the receptor. Previously, we documented that a GR

Indexed as

HypertensionReceptors, GlucocorticoidAnimalsAortaBlood PressureEpoxide HydrolasesFatty Acids, UnsaturatedMaleMutationRatsSodium Chloride, DietaryEpoxide HydrolasesFatty Acids, UnsaturatedReceptors, GlucocorticoidSodium Chloride, DietaryAdrenal gland hyperplasiaChrousos syndromeGlucocorticoid receptorHypertensionSoluble epoxide hydrolase

Identifiers

PMID39256246
PMCPMC11711871

What Socratic 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 Socratic graph.