Evidence map›Paper›PMID 30581820›Full record

ReviewFrontiers in cardiovascular medicine2018

Cell-Matrix Interactions and Matricrine Signaling in the Pathogenesis of Vascular Calcification.

David Ngai, Marsel Lino, Michelle P Bendeck

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  5. A mechanosensitive circuit of FAK, ROCK, and ERK controls biomineral growth and morphology in the sea urchin embryo.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  8. Review
  9. Article
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  12. Observational
  13. Article
  14. Article
  15. New insight of complement system in the process of vascular calcification.Journal of cellular and molecular medicine · 2023
    Review
  16. Review
  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

3 authors at 2 institutions in 1 country.

David NgaiDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.
Marsel LinoDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.
Michelle P BendeckDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.
Ted Rogers Centre for Heart Research · CAUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular calcification is a complex pathological process occurring in patients with atherosclerosis, type 2 diabetes, and chronic kidney disease. The extracellular matrix, via matricrine-receptor signaling plays important roles in the pathogenesis of calcification. Calcification is mediated by osteochondrocytic-like cells that arise from transdifferentiating vascular smooth muscle cells. Recent advances in our understanding of the plasticity of vascular smooth muscle cell and other cells of mesenchymal origin have furthered our understanding of how these cells transdifferentiate into osteochondrocytic-like cells in response to environmental cues. In the present review, we examine the role of the extracellular matrix in the regulation of cell behavior and differentiation in the context of vascular calcification. In pathological calcification, the extracellular matrix not only provides a scaffold for mineral deposition, but also acts as an active signaling entity. In recent years, extracellular matrix components have been shown to influence cellular signaling through matrix receptors such as the discoidin domain receptor family, integrins, and elastin receptors, all of which can modulate osteochondrocytic differentiation and calcification. Changes in extracellular matrix stiffness and composition are detected by these receptors which in turn modulate downstream signaling pathways and cytoskeletal dynamics, which are critical to osteogenic differentiation. This review will focus on recent literature that highlights the role of cell-matrix interactions and how they influence cellular behavior, and osteochondrocytic transdifferentiation in the pathogenesis of cardiovascular calcification.

Indexed as

collagencytoskeletondiscoidin domain receptorextracellular matrixintegrinmechanotransductionosteogenesisvascular calcification

Identifiers

PMID30581820
PMCPMC6292870
OpenAlexW2904523424

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.