Evidence map›Paper›PMID 34831306›Full record

ArticleCells2021

Zinc Ameliorates the Osteogenic Effects of High Glucose in Vascular Smooth Muscle Cells.

Laura A Henze, Misael Estepa, Burkert Pieske, Florian Lang, Kai-Uwe Eckardt, Ioana Alesutan, Jakob Voelkl

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Hypotaurine Reduces Glucose-Mediated Vascular Calcification.Acta physiologica (Oxford, England) · 2025
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. 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

7 authors at 4 institutions in 2 countries.

Laura A HenzeDepartment of Internal Medicine and Cardiology, Charité-Universitätsmedizin Berlin, Campus Virchow-Klinikum, 13353 Berlin, Germany.
Misael EstepaDepartment of Internal Medicine and Cardiology, Charité-Universitätsmedizin Berlin, Campus Virchow-Klinikum, 13353 Berlin, Germany.
Burkert PieskeDepartment of Internal Medicine and Cardiology, Charité-Universitätsmedizin Berlin, Campus Virchow-Klinikum, 13353 Berlin, Germany.
Florian LangDepartment of Vegetative and Clinical Physiology, Eberhard Karls University Tübingen, 72076 Tübingen, Germany.
Kai-Uwe EckardtDepartment of Nephrology and Medical Intensive Care, Charité-Universitätsmedizin Berlin, 13353 Berlin, Germany.
Ioana AlesutanInstitute for Physiology and Pathophysiology, Johannes Kepler University Linz, 4040 Linz, Austria.
Jakob VoelklDepartment of Nephrology and Medical Intensive Care, Charité-Universitätsmedizin Berlin, 13353 Berlin, Germany.
Charité - Universitätsmedizin Berlin · DEGerman Centre for Cardiovascular Research · DEJohannes Kepler University of Linz · ATUniversity of Tübingen · DE

Funding

Berlin Institute of Health N/ADeutsche Forschungsgemeinschaft AL2054/1-1, VO2259/2-1Deutsches Zentrum für Herz-Kreislaufforschung N/AElse Kröner-Fresenius-Stiftung N/A
6 · The paper itself

Abstract

In diabetic patients, medial vascular calcification is common and associated with increased cardiovascular mortality. Excessive glucose concentrations can activate the nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-kB) and trigger pro-calcific effects in vascular smooth muscle cells (VSMCs), which may actively augment vascular calcification. Zinc is able to mitigate phosphate-induced VSMC calcification. Reduced serum zinc levels have been reported in diabetes mellitus. Therefore, in this study the effects of zinc supplementation were investigated in primary human aortic VSMCs exposed to excessive glucose concentrations. Zinc treatment was found to abrogate the stimulating effects of high glucose on VSMC calcification. Furthermore, zinc was found to blunt the increased expression of osteogenic and chondrogenic markers in high glucose-treated VSMCs. High glucose exposure was shown to activate NF-kB in VSMCs, an effect that was blunted by additional zinc treatment. Zinc was further found to increase the expression of TNFα-induced protein 3 (TNFAIP3) in high glucose-treated VSMCs. The silencing of TNFAIP3 was shown to abolish the protective effects of zinc on high glucose-induced NF-kB-dependent transcriptional activation, osteogenic marker expression, and the calcification of VSMCs. Silencing of the zinc-sensing receptor G protein-coupled receptor 39 (GPR39) was shown to abolish zinc-induced

Indexed as

AortaBiomarkersGene Expression RegulationGene SilencingGlucoseHumansMuscle, Smooth, VascularMyocytes, Smooth MuscleNF-kappa BOsteogenesisRNA, MessengerZincBiomarkersGlucoseNF-kappa BRNA, MessengerZincdiabetes mellitusGPR39high glucoseNF-kBosteogenic transitionvascular calcificationvascular smooth muscle cellszinc

Identifiers

PMID34831306
PMCPMC8623153
OpenAlexW3212517930

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.