Evidence map›Paper›PMID 29238011›Full record

ReviewJournal of atherosclerosis and thrombosis2018

Plaque Calcification During Atherosclerosis Progression and Regression.

Atsushi Shioi, Yuji Ikari

Open access · diamondAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of atherosclerosis and thrombosis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed, 2 pooled it
15.1field-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

140 citing papers in PubMed, 2 syntheses or guidelines pooled it, 258 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Genetic silencing of KChannels (Austin, Tex.) · 2025
    Article
  10. Review
  11. Article
  12. Review
  13. Preclinical evaluation of high-resolution CT,European journal of nuclear medicine and molecular imaging · 2025
    Article
  14. Review
  15. Article
  16. Observational
  17. Article
  18. Article
  19. Review
  20. Observational

80 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

2 authors at 2 institutions in 1 country.

Atsushi ShioiDepartment of Vascular Medicine, Osaka City University Graduate School of Medicine.
Yuji IkariDepartment of Cardiovascular Medicine, Tokai University School of Medicine.
Osaka City University · JPTokai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Plaque calcification develops by the inflammation-dependent mechanisms involved in progression and regression of atherosclerosis. Macrophages can undergo two distinct polarization states, that is, pro-inflammatory M1 phenotype in progression and anti-inflammatory M2 phenotype in regression. In plaque progression, predominant M1 macrophages promote the initial calcium deposition within the necrotic core of the lesions, called as microcalcification, through not only vesicle-mediated mineralization as the result of apoptosis of macrophages and vascular smooth muscle cells (VSMCs), but also VSMC differentiation into early phase osteoblasts. On the other hand, in plaque regression M2 macrophages are engaged in the healing response to plaque inflammation. In association with the resolution of chronic inflammation, M2 macrophages may facilitate macroscopic calcium deposition, called as macrocalcification, through induction of osteoblastic differentiation and maturation of VSMCs. Oncostatin M, which has been shown to promote osteoblast differentiation in bone, may play a pivotal role in the development of plaque calcification. Clinically, two types of plaque calcification have distinct implications. Macrocalcification leads to plaque stability, while microcalcification is more likely to be associated with plaque rupture. Statin therapy, which reduces cardiovascular mortality, has been shown to exert its dual actions on plaque morphology, that is, regression of atheroma and increment of macroscopic calcium deposits. Statins may facilitate the healing process against plaque inflammation by enhancing M2 polarization of macrophages. Vascular calcification has pleiotropic properties as pro-inflammatory "microcalcification" and anti-inflammatory "macrocalcification". The molecular mechanisms of this process in relation with plaque progression as well as plaque regression should be intensively elucidated.

Indexed as

AnimalsApoptosisCell DifferentiationDisease ProgressionEndoplasmic Reticulum StressHumansHydroxymethylglutaryl-CoA Reductase InhibitorsInflammationMacrophagesMuscle, Smooth, VascularOncostatin MOsteoblastsPhenotypePlaque, AtheroscleroticPositron-Emission TomographyVascular CalcificationHydroxymethylglutaryl-CoA Reductase InhibitorsOncostatin MInflammationMacrocalcificationMacrophage polarizationMicrocalcification

Identifiers

PMID29238011
PMCPMC5906181
OpenAlexW2773133015

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.