Evidence map›Paper›PMID 31330917›Full record

ArticleToxins2019

Sclerostin as Regulatory Molecule in Vascular Media Calcification and the Bone-Vascular Axis.

Annelies De Maré, Stuart Maudsley, Abdelkrim Azmi, Jhana O Hendrickx, Britt Opdebeeck, Ellen Neven, Patrick C D'Haese, Anja Verhulst

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Toxins, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
7.8field-weighted citation impact, top 2% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 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

8 authors at 1 institution in 1 country.

Annelies De MaréLaboratory of Pathophysiology, Department of Biomedical Sciences, University of Antwerp, 2610 Wilrijk, Belgium.
Stuart MaudsleyReceptor Biology Lab, Department of Biomedical Sciences, University of Antwerp, 2610 Wilrijk, Belgium.
Abdelkrim AzmiTranslational Neurobiology Group, VIB Center for Molecular Neurology, University of Antwerp, 2610 Wilrijk, Belgium.
Jhana O HendrickxReceptor Biology Lab, Department of Biomedical Sciences, University of Antwerp, 2610 Wilrijk, Belgium.ORCID 0000-0001-7639-2926
Britt OpdebeeckLaboratory of Pathophysiology, Department of Biomedical Sciences, University of Antwerp, 2610 Wilrijk, Belgium.
Ellen NevenLaboratory of Pathophysiology, Department of Biomedical Sciences, University of Antwerp, 2610 Wilrijk, Belgium.
Patrick C D'HaeseLaboratory of Pathophysiology, Department of Biomedical Sciences, University of Antwerp, 2610 Wilrijk, Belgium. patrick.dhaese@uantwerpen.be.
Anja VerhulstLaboratory of Pathophysiology, Department of Biomedical Sciences, University of Antwerp, 2610 Wilrijk, Belgium.
University of Antwerp · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sclerostin is a well-known inhibitor of bone formation that acts on Wnt/β-catenin signaling. This manuscript considers the possible role of sclerostin in vascular calcification, a process that shares many similarities with physiological bone formation. Rats were exposed to a warfarin-containing diet to induce vascular calcification. Vascular smooth muscle cell transdifferentiation, vascular calcification grade, and bone histomorphometry were examined. The presence and/or production of sclerostin was investigated in serum, aorta, and bone. Calcified human aortas were investigated to substantiate clinical relevance. Warfarin-exposed rats developed vascular calcifications in a time-dependent manner which went along with a progressive increase in serum sclerostin levels. Both osteogenic and adipogenic pathways were upregulated in calcifying vascular smooth muscle cells, as well as sclerostin mRNA and protein levels. Evidence for the local vascular action of sclerostin was found both in human and rat calcified aortas. Warfarin exposure led to a mildly decreased bone and mineralized areas. Osseous sclerostin production and bone turnover did not change significantly. This study showed local production of sclerostin in calcified vessels, which may indicate a negative feedback mechanism to prevent further calcification. Furthermore, increased levels of serum sclerostin, probably originating from excessive local production in calcified vessels, may contribute to the linkage between vascular pathology and impaired bone mineralization.

Indexed as

Adaptor Proteins, Signal TransducingAdipogenesisAnimalsArteriesBone and BonesBone Morphogenetic ProteinsCalciumCell DifferentiationGenetic MarkersHumansMaleMyocytes, Smooth MuscleOsteogenesisRats, WistarRNA, MessengerVascular CalcificationAdaptor Proteins, Signal TransducingBone Morphogenetic ProteinsCalciumGenetic MarkersRNA, MessengerSOST protein, humanSost protein, ratWarfarinbone diseasechronic kidney diseasemineral abnormalitiesrat modelvascular calcification

Identifiers

PMID31330917
PMCPMC6669501
OpenAlexW2962747654

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.