Evidence map›Paper›PMID 29514202›Full record

ReviewCardiovascular research2018

Role of smooth muscle cells in vascular calcification: implications in atherosclerosis and arterial stiffness.

Andrew L Durham, Mei Y Speer, Marta Scatena, Cecilia M Giachelli, Catherine M Shanahan

Open access · hybridAbstract readReview
In one paragraph

Review in Cardiovascular research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 611 papers.

0numbers the graph read from it
0cells of the map it votes in
611citing papers in PubMed
48.0field-weighted citation impact, top 1% 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

611 citing papers in PubMed, 1,042 citations in OpenAlex.

  1. Review
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  6. Review
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  9. Review
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  11. Cellular crosstalk between endothelial and vascular smooth muscle cells via the BACH1/COL3A1 axis promotes vascular calcification in chronic kidney disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  12. Article
  13. Article
  14. Screening for candidate genes and cell populations associated with atherosclerotic calcification using single-cell RNA sequencing.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

551 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

5 authors at 2 institutions in 2 countries.

Andrew L DurhamDivision of Cardiology, James Black Centre, Kings College London, Denmark Hill, London, SE5 9NU, UK.
Mei Y SpeerDepartment of Bioengineering, University of Washington, Seattle, WA 98195, USA.
Marta ScatenaDepartment of Bioengineering, University of Washington, Seattle, WA 98195, USA.
Cecilia M GiachelliDepartment of Bioengineering, University of Washington, Seattle, WA 98195, USA.
Catherine M ShanahanDivision of Cardiology, James Black Centre, Kings College London, Denmark Hill, London, SE5 9NU, UK.
University of Washington · USKing's College London · GB

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Sakeneh Zraika · 1986 to 2026
$41.4M
Mechanisms of vascular and valvular calcificationR35HL139602 · NHLBI · UNIVERSITY OF WASHINGTON · PI GIACHELLI, CECILIA M · 2018 to 2023
$5.6M
Calcification and Vascular Cell DifferentiationR01HL081785 · NHLBI · UNIVERSITY OF WASHINGTON · PI GIACHELLI, CECILIA M · 2005 to 2017
$3.7M
RANK-RANKL and Vascular Complications in Chronic Kidney DiseaseR01DK094434 · NIDDK · UNIVERSITY OF WASHINGTON · PI ROSENFELD, MICHAEL E · 2012 to 2016
$2.5M
Role of Osteoclastogenesis in Calcific Aortic Valve DiseaseR01HL114611 · NHLBI · UNIVERSITY OF WASHINGTON · PI GIACHELLI, CECILIA M · 2012 to 2016
$1.9M
British Heart Foundation RG/17/2/32808NHLBI NIH HHS R01 HL081785NHLBI NIH HHS R01 HL114611NHLBI NIH HHS R35 HL139602NIDDK NIH HHS P30 DK017047NIDDK NIH HHS R01 DK094434
6 · The paper itself

Abstract

Vascular calcification is associated with a significant increase in all-cause mortality and atherosclerotic plaque rupture. Calcification has been determined to be an active process driven in part by vascular smooth muscle cell (VSMC) transdifferentiation within the vascular wall. Historically, VSMC phenotype switching has been viewed as binary, with the cells able to adopt a physiological contractile phenotype or an alternate 'synthetic' phenotype in response to injury. More recent work, including lineage tracing has however revealed that VSMCs are able to adopt a number of phenotypes, including calcific (osteogenic, chondrocytic, and osteoclastic), adipogenic, and macrophagic phenotypes. Whilst the mechanisms that drive VSMC differentiation are still being elucidated it is becoming clear that medial calcification may differ in several ways from the intimal calcification seen in atherosclerotic lesions, including risk factors and specific drivers for VSMC phenotype changes and calcification. This article aims to compare and contrast the role of VSMCs in driving calcification in both atherosclerosis and in the vessel media focusing on the major drivers of calcification, including aging, uraemia, mechanical stress, oxidative stress, and inflammation. The review also discusses novel findings that have also brought attention to specific pro- and anti-calcifying proteins, extracellular vesicles, mitochondrial dysfunction, and a uraemic milieu as major determinants of vascular calcification.

Indexed as

Plaque, AtheroscleroticAnimalsArteriesAtherosclerosisHumansMuscle, Smooth, VascularMyocytes, Smooth MusclePhenotypeSignal TransductionVascular CalcificationVascular Stiffness

Identifiers

PMID29514202
PMCPMC5852633
OpenAlexW2790654167

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.