Evidence map›Paper›PMID 34769044›Full record

ArticleInternational journal of molecular sciences2021

Endothelial Contribution to Warfarin-Induced Arterial Media Calcification in Mice.

Geoffrey Van den Bergh, Sofie De Moudt, Astrid Van den Branden, Ellen Neven, Hanne Leysen, Stuart Maudsley, Guido R Y De Meyer, Patrick D'Haese, Anja Verhulst

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Towards a better understanding of arterial calcification disease progression in CKD: investigation of early pathological alterations.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023
    Article
  7. Article
  8. 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

9 authors at 1 institution in 1 country.

Geoffrey Van den BerghLaboratory of Pathophysiology, University of Antwerp, 2610 Wilrijk, Belgium.
Sofie De MoudtLaboratory of Physiopharmacology, University of Antwerp, 2610 Wilrijk, Belgium.
Astrid Van den BrandenLaboratory of Pathophysiology, University of Antwerp, 2610 Wilrijk, Belgium.ORCID 0000-0001-6325-4997
Ellen NevenLaboratory of Pathophysiology, University of Antwerp, 2610 Wilrijk, Belgium.
Hanne LeysenReceptor Biology Laboratory, University of Antwerp, 2610 Wilrijk, Belgium.ORCID 0000-0002-5852-9033
Stuart MaudsleyReceptor Biology Laboratory, University of Antwerp, 2610 Wilrijk, Belgium.ORCID 0000-0002-1868-184X
Guido R Y De MeyerLaboratory of Physiopharmacology, University of Antwerp, 2610 Wilrijk, Belgium.ORCID 0000-0003-3848-8702
Patrick D'HaeseLaboratory of Pathophysiology, University of Antwerp, 2610 Wilrijk, Belgium.ORCID 0000-0003-1463-6571
Anja VerhulstLaboratory of Pathophysiology, University of Antwerp, 2610 Wilrijk, Belgium.
University of Antwerp · BE

Funding

Research Foundation - Flanders 1S18818NUniversity of Antwerp GOA-BOF grant 33932
6 · The paper itself

Abstract

Arterial media calcification (AMC) is predominantly regulated by vascular smooth muscle cells (VSMCs), which transdifferentiate into pro-calcifying cells. In contrast, there is little evidence for endothelial cells playing a role in the disease. The current study investigates cellular functioning and molecular pathways underlying AMC, respectively by, an ex vivo isometric organ bath set-up to explore the interaction between VSMCs and ECs and quantitative proteomics followed by functional pathway interpretation. AMC development, which was induced in mice by dietary warfarin administration, was proved by positive Von Kossa staining and a significantly increased calcium content in the aorta compared to that of control mice. The ex vivo organ bath set-up showed calcified aortic segments to be significantly more sensitive to phenylephrine induced contraction, compared to control segments. This, together with the fact that calcified segments as compared to control segments, showed a significantly smaller contraction in the absence of extracellular calcium, argues for a reduced basal NO production in the calcified segments. Moreover, proteomic data revealed a reduced eNOS activation to be part of the vascular calcification process. In summary, this study identifies a poor endothelial function, next to classic pro-calcifying stimuli, as a possible initiator of arterial calcification.

Indexed as

AnimalsAortaCalcification, PhysiologicCalciumCell TransdifferentiationEndothelial CellsMaleMiceMice, Inbred DBAMuscle, Smooth, VascularMyocytes, Smooth MuscleOsteogenesisTunica MediaVascular CalcificationWarfarinCalciumWarfarinendothelial cellsnitric oxideorgan bathsvascular calcificationvascular smooth muscle cells

Identifiers

PMID34769044
PMCPMC8583869
OpenAlexW3209248886

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.