Evidence map›Paper›PMID 38892126›Full record

ArticleInternational journal of molecular sciences2024

Ablation of Vitamin D Signaling in Cardiomyocytes Leads to Functional Impairment and Stimulation of Pro-Inflammatory and Pro-Fibrotic Gene Regulatory Networks in a Left Ventricular Hypertrophy Model in Mice.

Ana Zupcic, Nejla Latic, Mhaned Oubounyt, Alice Ramesova, Geert Carmeliet, Jan Baumbach, Maria L Elkjaer, Reinhold G Erben

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

8 authors.

Ana ZupcicDepartment of Biomedical Sciences, University of Veterinary Medicine, 1210 Vienna, Austria.
Nejla LaticDepartment of Biomedical Sciences, University of Veterinary Medicine, 1210 Vienna, Austria.ORCID 0000-0001-5635-5175
Mhaned OubounytInstitute for Computational Systems Biology, University of Hamburg, Albert-Einstein-Ring 8-10, 22761 Hamburg, Germany.
Alice RamesovaDepartment of Biomedical Sciences, University of Veterinary Medicine, 1210 Vienna, Austria.ORCID 0000-0001-7482-7818
Geert CarmelietDepartment of Chronic Diseases, Metabolism and Ageing, 3000 Leuven, Belgium.
Jan BaumbachInstitute for Computational Systems Biology, University of Hamburg, Albert-Einstein-Ring 8-10, 22761 Hamburg, Germany.
Maria L ElkjaerInstitute for Computational Systems Biology, University of Hamburg, Albert-Einstein-Ring 8-10, 22761 Hamburg, Germany.ORCID 0000-0002-8596-142X
Reinhold G ErbenDepartment of Biomedical Sciences, University of Veterinary Medicine, 1210 Vienna, Austria.ORCID 0000-0003-0801-6958

Funding

FWF Austrian Science Fund P26534-B13German Federal Ministry of Education and Research (BMBF) 031L0309B
6 · The paper itself

Abstract

The association between vitamin D deficiency and cardiovascular disease remains a controversial issue. This study aimed to further elucidate the role of vitamin D signaling in the development of left ventricular (LV) hypertrophy and dysfunction. To ablate the vitamin D receptor (VDR) specifically in cardiomyocytes, VDR

Indexed as

Disease Models, AnimalFibrosisGene Regulatory NetworksHypertrophy, Left VentricularMice, KnockoutMyocytes, CardiacReceptors, CalcitriolSignal TransductionVitamin DAnimalsInflammationMaleMiceReceptors, CalcitriolVitamin Dcardiomyocytesfibrosisinflammationleft ventricular hypertrophyspatial transcriptomicsvitamin Dvitamin D receptor

Identifiers

PMID38892126
PMCPMC11172934

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.