Evidence map›Paper›PMID 26985381›Full record

ArticleClinical kidney journal2016

Calcifying circulating cells: an uncharted area in the setting of vascular calcification in CKD patients.

Giuseppe Cianciolo, Irene Capelli, Maria Cappuccilli, Roberto Schillaci, Mario Cozzolino, Gaetano La Manna

Open access · goldAbstract read
In one paragraph

Article in Clinical kidney journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 30 citations in OpenAlex.

  1. A new SOFrontiers in physiology · 2025
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  14. Research Models for Studying Vascular Calcification.International journal of molecular sciences · 2020
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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

6 authors at 2 institutions in 1 country.

Giuseppe CiancioloNephrology, Dialysis and Renal Transplant Unit, S. Orsola Hospital, Department of Experimental Diagnostic and Specialty Medicine (DIMES) , University of Bologna , Bologna , Italy.
Irene CapelliNephrology, Dialysis and Renal Transplant Unit, S. Orsola Hospital, Department of Experimental Diagnostic and Specialty Medicine (DIMES) , University of Bologna , Bologna , Italy.
Maria CappuccilliNephrology, Dialysis and Renal Transplant Unit, S. Orsola Hospital, Department of Experimental Diagnostic and Specialty Medicine (DIMES) , University of Bologna , Bologna , Italy.
Roberto SchillaciNephrology, Dialysis and Renal Transplant Unit, S. Orsola Hospital, Department of Experimental Diagnostic and Specialty Medicine (DIMES) , University of Bologna , Bologna , Italy.
Mario CozzolinoNephrology and Dialysis, S. Paolo Hospital, Department of Health Sciences (DISS) , University of Milan , Milan , Italy.
Gaetano La MannaNephrology, Dialysis and Renal Transplant Unit, S. Orsola Hospital, Department of Experimental Diagnostic and Specialty Medicine (DIMES) , University of Bologna , Bologna , Italy.
University of Bologna · ITOspedale San Paolo · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular calcification, occurring during late-stage vascular and valvular disease, is highly associated with chronic kidney disease-mineral and bone disorders (CKD-MBD), representing a major risk factor for cardiovascular morbidity and mortality. The hallmark of vascular calcification, which involves both media and intima, is represented by the activation of cells committed to an osteogenic programme. Several studies have analysed the role of circulating calcifying cells (CCCs) in vascular calcification. CCCs are bone marrow (BM)-derived cells with an osteogenic phenotype, participating in intima calcification processes and defined by osteocalcin and bone alkaline phosphatase expression. The identification of CCCs in diabetes and atherosclerosis is the most recent, intriguing and yet uncharted chapter in the scenario of the bone-vascular axis. Whether osteogenic shift occurs in the BM, the bloodstream or both, is not known, and also the factors promoting CCC formation have not been identified. However, it is possible to recognize a common pathogenic commitment of inflammation in atherosclerosis and diabetes, in which metabolic control may also have a role. Currently available studies in patients without CKD did not find an association of CCCs with markers of bone metabolism. Preliminary data on CKD patients indicate an implication of mineral bone disease in vascular calcification, as a consequence of functional and anatomic integrity interruption of BM niches. Given the pivotal role that parathyroid hormone and osteoblasts play in regulating expansion, mobilization and homing of haematopoietic stem/progenitors cells, CKD-MBD could promote CCC formation.

Indexed as

atherosclerosiscalcifying circulating cellschronic kidney disease-mineral and bone disordersmineral metabolismvascular calcification

Identifiers

PMID26985381
PMCPMC4792620
OpenAlexW2258896700

What OpenQuestion holds

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LicenceCC BY-NC
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.