Evidence map›Paper›PMID 18080808›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2008

Mineral chaperones: a role for fetuin-A and osteopontin in the inhibition and regression of pathologic calcification.

Willi Jahnen-Dechent, Cora Schäfer, Markus Ketteler, Marc D McKee

2 registry-linked trialsAbstract readReview
PubMed Publisher
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
4.8field-weighted citation impact, top 5% 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.

NCT00694824 completednot on this map

Traditional and Not Traditional Risk Factors in Appearance and Progression of Vascular Calcification in Haemodialysis Patients.

TypeobservationalSponsorIRCCS Azienda Ospedaliero-Universitaria di BolognaRan2004 to 2008Enrolled253ConditionsChronic Kidney Failure, Inflammation, Vascular Calcification
NCT02635373 unknown statusnot on this mapstarted 2015, after this paper: background citation

European Calciphylaxis Registry Network

Typeobservational_patient_registrySponsorRWTH Aachen UniversityRan2015 to 2020Enrolled1,000ConditionsCalcific Uremic Arteriolopathy (CUA), Calciphylaxis
3 · Its place in the literature

Who cites it

71 citing papers in PubMed, 174 citations in OpenAlex.

  1. Effect of the phosphate binder sucroferric oxyhydroxide in dialysis patients on endogenous calciprotein particles, inflammation, and vascular cells.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023
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  7. The formation and function of calciprotein particles.Pflugers Archiv : European journal of physiology · 2025
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11 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 2 countries.

Willi Jahnen-DechentDepartment of Biomedical Engineering, Biointerface Laboratory, RWTH Aachen University Clinics, Pauwelsstrasse 30, 52074 Aachen, Germany. willi.jahnen@rwth-aachen.de
Cora Schäfer
Markus Ketteler
Marc D McKee
RWTH Aachen University · DEKlinikum Coburg · DEMcGill University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clinical nephrologists are well aware of the consequences of pathologic mineralization (calcification). Several studies have found a strong association between vascular and valvular mineralization and advanced or end-stage chronic kidney disease (CKD), with shorter survival times and increased morbidity. In the cardiology community, until quite recently, ectopic mineralization was considered harmless or even beneficial. Some still assume that atherosclerotic intima mineralization stabilizes atherosclerotic plaques, thus doing more good than harm. We suggest that vascular mineralization and indeed soft tissue mineralization in general may be a way in which the body deals with certain adverse situations involving local inflammation, associated tissue damage and tissue remodeling. Ectopic soft tissue mineralization resembles physiological bone mineralization in many ways. Markers of mineralizing bone also are present during soft tissue mineralization. We postulate that it may be possible to reverse soft tissue mineralization by applying selected principles of bone catabolism, namely mineral dissolution and phagocytosis. We consider putative strategies for therapeutic intervention to maximize the clearing of calcified debris particles. In particular, we discuss the roles of the plasma protein fetuin-A/alpha2HS-glycoprotein and the mineral-binding protein osteopontin in the prevention and possible regression of mineralization in disease.

Indexed as

Calcinosisalpha-2-HS-GlycoproteinAnimalsBlood ProteinsBone and BonesHumansKidney Failure, ChronicMacrophagesMineralsOsteopontinAHSG protein, humanalpha-2-HS-GlycoproteinBlood ProteinsMineralsOsteopontin

Identifiers

PMID18080808
OpenAlexW2030057384

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.