Evidence map›Paper›PMID 30700131›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2019

Potential Role of H-Ferritin in Mitigating Valvular Mineralization.

Katalin Éva Sikura, László Potor, Tamás Szerafin, Abolfazl Zarjou, Anupam Agarwal, Paolo Arosio, Maura Poli, Zoltán Hendrik, Gábor Méhes, Melinda Oros and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
28.5field-weighted citation impact, top 1% 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

19 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Iron in Vascular Calcification: Pro-Calcific Agent or Protective Modulator?International journal of molecular sciences · 2025
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  3. Review
  4. The Role of Iron in Calciphylaxis-A Current Review.Journal of clinical medicine · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Iron in Cardiovascular Disease: Challenges and Potentials.Frontiers in cardiovascular medicine · 2021
    Review
  15. Review
  16. Vascular Endothelial Cells and Innate Immunity.Arteriosclerosis, thrombosis, and vascular biology · 2020
    Review
  17. Article
  18. Review
  19. 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

15 authors at 3 institutions in 2 countries.

Katalin Éva SikuraFrom the HAS-UD Vascular Biology and Myocardial Pathophysiology Research Group, Hungarian, Academy of Sciences, Debrecen (K.É.S., L.P., M.O., N.P., G.B., J.B.), Faculty of Medicine, University of Debrecen, Hungary.
László PotorFrom the HAS-UD Vascular Biology and Myocardial Pathophysiology Research Group, Hungarian, Academy of Sciences, Debrecen (K.É.S., L.P., M.O., N.P., G.B., J.B.), Faculty of Medicine, University of Debrecen, Hungary.
Tamás SzerafinDepartments of Medicine (K.É.S., L.P., T.S., M.O., N.P., I.F., J.B.), Faculty of Medicine, University of Debrecen, Hungary.
Abolfazl ZarjouDepartment of Medicine, Division of Nephrology, Nephrology Research and Training Center and Center for Free Radical Biology, University of Alabama at Birmingham (A.Z., A.A.).
Anupam AgarwalDepartment of Medicine, Division of Nephrology, Nephrology Research and Training Center and Center for Free Radical Biology, University of Alabama at Birmingham (A.Z., A.A.).
Paolo ArosioDepartment of Molecular and Translational Medicine, University of Brescia, Italy (P.A., M.P.).
Maura PoliDepartment of Molecular and Translational Medicine, University of Brescia, Italy (P.A., M.P.).
Zoltán HendrikPathology (Z.H., G.M., N.P.), Faculty of Medicine, University of Debrecen, Hungary.
Gábor MéhesPathology (Z.H., G.M., N.P.), Faculty of Medicine, University of Debrecen, Hungary.
Melinda OrosFrom the HAS-UD Vascular Biology and Myocardial Pathophysiology Research Group, Hungarian, Academy of Sciences, Debrecen (K.É.S., L.P., M.O., N.P., G.B., J.B.), Faculty of Medicine, University of Debrecen, Hungary.
Niké PostaFrom the HAS-UD Vascular Biology and Myocardial Pathophysiology Research Group, Hungarian, Academy of Sciences, Debrecen (K.É.S., L.P., M.O., N.P., G.B., J.B.), Faculty of Medicine, University of Debrecen, Hungary.
Lívia BekeFrom the HAS-UD Vascular Biology and Myocardial Pathophysiology Research Group, Hungarian, Academy of Sciences, Debrecen (K.É.S., L.P., M.O., N.P., G.B., J.B.), Faculty of Medicine, University of Debrecen, Hungary.
Ibolya FürtösDepartments of Medicine (K.É.S., L.P., T.S., M.O., N.P., I.F., J.B.), Faculty of Medicine, University of Debrecen, Hungary.
György BallaFrom the HAS-UD Vascular Biology and Myocardial Pathophysiology Research Group, Hungarian, Academy of Sciences, Debrecen (K.É.S., L.P., M.O., N.P., G.B., J.B.), Faculty of Medicine, University of Debrecen, Hungary.
József BallaFrom the HAS-UD Vascular Biology and Myocardial Pathophysiology Research Group, Hungarian, Academy of Sciences, Debrecen (K.É.S., L.P., M.O., N.P., G.B., J.B.), Faculty of Medicine, University of Debrecen, Hungary.
University of Debrecen · HUHungarian Academy of Sciences · HUPediatric Nephrology of Alabama · US

Funding

Targeting Ferritin in Vascular Calcification Associated With CKDK08HL140294 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ZARJOU, ABOLFAZL · 2018 to 2022
$841k
NHLBI NIH HHS K08 HL140294
6 · The paper itself

Abstract

Objective- Calcific aortic valve disease is a prominent finding in elderly and in patients with chronic kidney disease. We investigated the potential role of iron metabolism in the pathogenesis of calcific aortic valve disease. Approach and Results- Cultured valvular interstitial cells of stenotic aortic valve with calcification from patients undergoing valve replacement exhibited significant susceptibility to mineralization/osteoblastic transdifferentiation in response to phosphate. This process was abrogated by iron via induction of H-ferritin as reflected by lowering ALP and osteocalcin secretion and preventing extracellular calcium deposition. Cellular phosphate uptake and accumulation of lysosomal phosphate were decreased. Accordingly, expression of phosphate transporters Pit1 and Pit2 were repressed. Translocation of ferritin into lysosomes occurred with high phosphate-binding capacity. Importantly, ferritin reduced nuclear accumulation of RUNX2 (Runt-related transcription factor 2), and as a reciprocal effect, it enhanced nuclear localization of transcription factor Sox9 (SRY [sex-determining region Y]-box 9). Pyrophosphate generation was also increased via upregulation of ENPP2 (ectonucleotide pyrophosphatase/phosphodiesterase-2).

Indexed as

Aortic ValveAortic Valve StenosisApoferritinsBiological TransportCell NucleusCells, CulturedCore Binding Factor Alpha 1 SubunitEndothelial CellsGene Expression RegulationInterleukin-1betaIon ChannelsIronLysophospholipase DLysosomesPhosphatesPhosphoric Diester Hydrolases1,2-dithiol-3-thioneApoferritinsCore Binding Factor Alpha 1 SubunitInterleukin-1betaIon ChannelsIronLysophospholipase DPhosphatesPhosphoric Diester HydrolasesRUNX2 protein, humanSOX9 protein, humanSOX9 Transcription FactorThionesThiophenesTumor Necrosis Factor-alphaarteriosclerosischronic kidney diseasephosphatestenosisvascular calcification

Identifiers

PMID30700131
PMCPMC6393195
OpenAlexW2913401366

What OpenQuestion holds

Textmetadata
LicenceTDM
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.