Evidence map›Paper›PMID 29643466›Full record

ArticleScientific reports2018

Etidronate prevents dystrophic cardiac calcification by inhibiting macrophage aggregation.

Carolin Bauer, Olivier le Saux, Viola Pomozi, Redouane Aherrahrou, Rene Kriesen, Stephanie Stölting, Annett Liebers, Thorsten Kessler, Heribert Schunkert, Jeanette Erdmann and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Considerations on the Development of Therapeutics in Vascular Calcification.Journal of cardiovascular development and disease · 2025
    Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. ABCC6, Pyrophosphate and Ectopic Calcification: Therapeutic Solutions.International journal of molecular sciences · 2021
    Review
  8. Article
  9. Review
  10. Article
  11. Article
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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

11 authors at 5 institutions in 2 countries.

Carolin BauerInstitute for Cardiogenetics, Universität zu Lübeck; DZHK (German Centre for Cardiovascular Research), Partner Site Hamburg/Kiel/Lübeck, Germany, University Heart Centre Lübeck, 23562, Lübeck, Germany.
Olivier le SauxDepartment of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI, USA.
Viola PomoziDepartment of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI, USA.
Redouane AherrahrouInstitute for Cardiogenetics, Universität zu Lübeck; DZHK (German Centre for Cardiovascular Research), Partner Site Hamburg/Kiel/Lübeck, Germany, University Heart Centre Lübeck, 23562, Lübeck, Germany.
Rene KriesenInstitute for Cardiogenetics, Universität zu Lübeck; DZHK (German Centre for Cardiovascular Research), Partner Site Hamburg/Kiel/Lübeck, Germany, University Heart Centre Lübeck, 23562, Lübeck, Germany.
Stephanie StöltingInstitute for Cardiogenetics, Universität zu Lübeck; DZHK (German Centre for Cardiovascular Research), Partner Site Hamburg/Kiel/Lübeck, Germany, University Heart Centre Lübeck, 23562, Lübeck, Germany.
Annett LiebersInstitute for Cardiogenetics, Universität zu Lübeck; DZHK (German Centre for Cardiovascular Research), Partner Site Hamburg/Kiel/Lübeck, Germany, University Heart Centre Lübeck, 23562, Lübeck, Germany.
Thorsten KesslerDeutsches Herzzentrum München, Technische Universität München and DZHK (German Centre for Cardiovascular Research); Partner Site Munich Heart Alliance, Technische Universität München, München, Germany.
Heribert SchunkertDeutsches Herzzentrum München, Technische Universität München and DZHK (German Centre for Cardiovascular Research); Partner Site Munich Heart Alliance, Technische Universität München, München, Germany.
Jeanette ErdmannInstitute for Cardiogenetics, Universität zu Lübeck; DZHK (German Centre for Cardiovascular Research), Partner Site Hamburg/Kiel/Lübeck, Germany, University Heart Centre Lübeck, 23562, Lübeck, Germany.
Zouhair AherrahrouInstitute for Cardiogenetics, Universität zu Lübeck; DZHK (German Centre for Cardiovascular Research), Partner Site Hamburg/Kiel/Lübeck, Germany, University Heart Centre Lübeck, 23562, Lübeck, Germany. zouhair.aherrahrou@uni-luebeck.de.
University of Lübeck · DEUniversität Hamburg · DEUniversity of Hawaiʻi at Mānoa · USDeutsches Herzzentrum München · DETechnical University of Munich · DE

Funding

TRPA1 Physiology in Diabetes, Metabolic Syndrome, and MetabolismP20GM113134 · NIGMS · UNIVERSITY OF HAWAII AT MANOA · PI Kathryn Jaques Schunke · 2017 to 2026
$21.5M
Pilot Project ProgramP30GM103341 · NIGMS · UNIVERSITY OF HAWAII AT MANOA · PI SHOHET, RALPH V. · 2012 to 2016
$5.5M
The role of ABCC6 in chronic and acute cardiovascular mineralizationR01HL108249 · NHLBI · UNIVERSITY OF HAWAII AT MANOA · PI BOISVERT, WILLIAM A, LE SAUX, OLIVIER · 2012 to 2015
$1.4M
NHLBI NIH HHS R01 HL108249NIGMS NIH HHS P20 GM113134NIGMS NIH HHS P30 GM103341
6 · The paper itself

Abstract

Cardiovascular calcification is associated with high risk of vascular disease. This involves macrophage infiltration of injured vascular tissue and osteoclast-related processes. Splenic monocytes from mice, that are predisposed (C3H) or resistant (B6) to calcification, were isolated and differentiated in vitro with M-CSF to generate macrophages, which aggregate to form multinucleated (MN) cells in the presence of RANKL. MN cell formation was significantly decreased in monocytes from resistant compared with calcifying mice. Conditioned media from C3H macrophages strongly induced calcification in vitro. However, medium from B6 macrophages inhibited calcification. An increase in ICAM-1 was detected in conditioned media from C3H macrophages compared with B6, suggesting a key role for this molecule in calcification processes. Due to natural genetic loss of Abcc6, the causal gene for cardiac calcification, C3H mice have reduced plasma levels of inorganic pyrophosphate (PPi), a potential calcification inhibitor. Supplementation of C3H mice with PPi or Etidronate prevented but did not completely reverse cardiac calcification. Our data provide strong evidence of the pathogenesis of macrophages and MNs during tissue calcification and suggest PPi or its analogue Etidronate as a potential inhibitor of MN formation and calcification. Furthermore, the adhesion molecule ICAM-1 was shown to play a key role in calcification.

Indexed as

AnimalsBone Density Conservation AgentsCalcinosisCardiovascular DiseasesCell AggregationCells, CulturedDiphosphatesEtidronic AcidIntercellular Adhesion Molecule-1MacrophagesMice, Inbred C3HMice, Inbred C57BLBone Density Conservation AgentsDiphosphatesEtidronic AcidIntercellular Adhesion Molecule-1

Identifiers

PMID29643466
PMCPMC5895639
OpenAlexW2797204272

What OpenQuestion 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 OpenQuestion graph.