Evidence map›Paper›PMID 32885586›Full record

ArticleJournal of cellular and molecular medicine2020

Pyrophosphate therapy prevents trauma-induced calcification in the mouse model of neurogenic heterotopic ossification.

Natália Tőkési, Eszter Kozák, Krisztina Fülöp, Dóra Dedinszki, Nikolett Hegedűs, Bálint Király, Krisztián Szigeti, Kitti Ajtay, Zoltán Jakus, Jeremy Zaworski and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

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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

13 authors at 3 institutions in 2 countries.

Natália TőkésiInstitute of Enzymology, Research Center for Natural Sciences, Hungarian Academy of Sciences Centre of Excellence, Budapest, Hungary.
Eszter KozákInstitute of Enzymology, Research Center for Natural Sciences, Hungarian Academy of Sciences Centre of Excellence, Budapest, Hungary.
Krisztina FülöpInstitute of Enzymology, Research Center for Natural Sciences, Hungarian Academy of Sciences Centre of Excellence, Budapest, Hungary.
Dóra DedinszkiInstitute of Enzymology, Research Center for Natural Sciences, Hungarian Academy of Sciences Centre of Excellence, Budapest, Hungary.
Nikolett HegedűsDepartment of Biophysics and Radiation Biology, Semmelweis University, Budapest, Hungary.
Bálint KirályDepartment of Biophysics and Radiation Biology, Semmelweis University, Budapest, Hungary.
Krisztián SzigetiDepartment of Biophysics and Radiation Biology, Semmelweis University, Budapest, Hungary.
Kitti AjtayDepartment of Physiology, Semmelweis University, Budapest, Hungary.
Zoltán JakusDepartment of Physiology, Semmelweis University, Budapest, Hungary.
Jeremy ZaworskiSorbonne Université, UPMC Univ Paris 06, Paris, France.
Emmanuel LetavernierSorbonne Université, UPMC Univ Paris 06, Paris, France.
Viola PomoziInstitute of Enzymology, Research Center for Natural Sciences, Hungarian Academy of Sciences Centre of Excellence, Budapest, Hungary.
András VáradiInstitute of Enzymology, Research Center for Natural Sciences, Hungarian Academy of Sciences Centre of Excellence, Budapest, Hungary.ORCID 0000-0002-2722-7120
Institute of Molecular Life Sciences · HUSemmelweis University · HUInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Trauma-induced calcification is the pathological consequence of complex injuries which often affect the central nervous system and other parts of the body simultaneously. We demonstrated by an animal model recapitulating the calcification of the above condition that adrenaline transmits the stress signal of brain injury to the calcifying tissues. We have also found that although the level of plasma pyrophosphate, the endogenous inhibitor of calcification, was normal in calcifying animals, it could not counteract the acute calcification. However, externally added pyrophosphate inhibited calcification even when it was administered after the complex injuries. Our finding suggests a potentially powerful clinical intervention of calcification triggered by polytrauma injuries which has no effective treatment.

Indexed as

Adrenergic AntagonistsAnimalsBrain Injuries, TraumaticCardiotoxinsDiphosphatesDisease Models, AnimalEpinephrineFemaleGene Expression RegulationMice, Inbred C57BLMuscle, SkeletalOssification, HeterotopicReceptors, AdrenergicVascular CalcificationX-Ray MicrotomographyAdrenergic AntagonistsCardiotoxinsDiphosphatesdiphosphoric acidEpinephrineReceptors, Adrenergicanimal modelsbone-brain-nervous system interactionsdisorders of calcium/phosphate metabolisminterventionpreclinical studies

Identifiers

PMID32885586
PMCPMC7579705
OpenAlexW3083436933

What OpenQuestion holds

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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.