Evidence map›Paper›PMID 25735207›Full record

ReviewPediatric nephrology (Berlin, Germany)2016

From skeletal to cardiovascular disease in 12 steps-the evolution of sclerostin as a major player in CKD-MBD.

Vincent M Brandenburg, Patrick D'Haese, Annika Deck, Djalila Mekahli, Björn Meijers, Ellen Neven, Pieter Evenepoel

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Circulating Sclerostin Levels Are Positively Related to Coronary Artery Disease Severity and Related Risk Factors.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
    Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Sclerostin and Vascular Pathophysiology.International journal of molecular sciences · 2020
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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 3 institutions in 2 countries.

Vincent M BrandenburgDepartment of Cardiology, University Hospital of the RWTH Aachen, Pauwelsstraße 30, 52057, Aachen, Germany. vincent.brandenburg@post.rwth-aachen.de.
Patrick D'HaeseLaboratory of Pathophysiology, Department of Biomedical Sciences, University of Antwerp, Wilrijk, Belgium.
Annika DeckDepartment of Cardiology, University Hospital of the RWTH Aachen, Pauwelsstraße 30, 52057, Aachen, Germany.
Djalila MekahliDepartment of Pediatric Nephrology, University Hospitals Leuven, Leuven, Belgium.
Björn MeijersDepartment of Immunology and Microbiology, Laboratory of Nephrology, University Hospitals Leuven, Leuven, Belgium.
Ellen NevenLaboratory of Pathophysiology, Department of Biomedical Sciences, University of Antwerp, Wilrijk, Belgium.
Pieter EvenepoelDepartment of Immunology and Microbiology, Laboratory of Nephrology, University Hospitals Leuven, Leuven, Belgium.
KU Leuven · BERWTH Aachen University · DEUniversity of Antwerp · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Canonical Wnt signaling activity contributes to physiological and adaptive bone mineralization and is an essential player in bone remodeling. Sclerostin is a prototypic soluble canonical Wnt signaling pathway inhibitor that is produced in osteocytes and blocks osteoblast differentiation and function. Therefore, sclerostin is a potent inhibitor of bone formation and mineralization. Accordingly, rodent sclerostin-deficiency models exhibit a strong bone phenotype. Moreover, blocking sclerostin represents a promising treatment perspective against osteoporosis. Beyond the bone field novel data definitely associate Wnt signaling in general and sclerostin in particular with ectopic extraosseous mineralization processes, as is evident in cardiovascular calcification or calciphylaxis. Uremia is characterized by parallel occurrence of disordered bone mineralization and accelerated cardiovascular calcification (chronic kidney disease - mineral and bone disorder, CKD-MBD), linking skeletal and cardiovascular disease-the so-called bone-vascular calcification paradox. In consequence, sclerostin may qualify as an emerging player in CKD-MBD. We present a stepwise review approach regarding the rapidly evolving field sclerostin participation in CKD-MBD. Starting from data originating in the classical bone field we look separately at three major areas of CKD-MBD: disturbed mineral metabolism, renal osteodystrophy, and uremic cardiovascular disease. Our review is intended to help the nephrologist revise the potential importance of sclerostin in CKD by focusing on how sclerostin research is gradually evolving from the classical osteoporosis niche into the area of CKD-MBD. In particular, we integrate the limited amount of available data in the context of pediatric nephrology.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsBone and BonesBone DensityBone DiseasesBone Morphogenetic ProteinsBone RemodelingCardiovascular DiseasesGenetic MarkersHumansRenal Insufficiency, ChronicSignal TransductionAdaptor Proteins, Signal TransducingBone Morphogenetic ProteinsGenetic MarkersSOST protein, humanBone mineralizationCardiovascular calcificationChronic kidney disease mineral and bone disorderSclerostinWnt signaling

Identifiers

PMID25735207
OpenAlexW1987693071

What OpenQuestion holds

Textmetadata
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.