Evidence map›Paper›PMID 32781528›Full record

ReviewBioengineering (Basel, Switzerland)2020

Mechanisms of the Osteogenic Switch of Smooth Muscle Cells in Vascular Calcification: WNT Signaling, BMPs, Mechanotransduction, and EndMT.

John Tyson, Kaylee Bundy, Cameron Roach, Hannah Douglas, Valerie Ventura, Mary Frances Segars, Olivia Schwartz, C LaShan Simpson

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

Review in Bioengineering (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.8field-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.

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

49 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Efficacy and safety of romosozumab in patients with chronic kidney disease and osteoporosis: a narrative review.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Considerations on the Development of Therapeutics in Vascular Calcification.Journal of cardiovascular development and disease · 2025
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
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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

8 authors at 1 institution in 1 country.

John TysonDepartment of Agricultural and Biological Engineering, Mississippi State University, Starkville, MS 39762, USA.
Kaylee BundyDepartment of Agricultural and Biological Engineering, Mississippi State University, Starkville, MS 39762, USA.
Cameron RoachDepartment of Agricultural and Biological Engineering, Mississippi State University, Starkville, MS 39762, USA.
Hannah DouglasDepartment of Agricultural and Biological Engineering, Mississippi State University, Starkville, MS 39762, USA.
Valerie VenturaDepartment of Agricultural and Biological Engineering, Mississippi State University, Starkville, MS 39762, USA.
Mary Frances SegarsDepartment of Agricultural and Biological Engineering, Mississippi State University, Starkville, MS 39762, USA.
Olivia SchwartzDepartment of Agricultural and Biological Engineering, Mississippi State University, Starkville, MS 39762, USA.
C LaShan SimpsonDepartment of Agricultural and Biological Engineering, Mississippi State University, Starkville, MS 39762, USA.
Mississippi State University · US

Funding

Mississippi Agricultural and Forestry Experiment Station, Mississippi State University XXXXXXX
6 · The paper itself

Abstract

Characterized by the hardening of arteries, vascular calcification is the deposition of hydroxyapatite crystals in the arterial tissue. Calcification is now understood to be a cell-regulated process involving the phenotypic transition of vascular smooth muscle cells into osteoblast-like cells. There are various pathways of initiation and mechanisms behind vascular calcification, but this literature review highlights the wingless-related integration site (WNT) pathway, along with bone morphogenic proteins (BMPs) and mechanical strain. The process mirrors that of bone formation and remodeling, as an increase in mechanical stress causes osteogenesis. Observing the similarities between the two may aid in the development of a deeper understanding of calcification. Both are thought to be regulated by the WNT signaling cascade and bone morphogenetic protein signaling and can also be activated in response to stress. In a pro-calcific environment, integrins and cadherins of vascular smooth muscle cells respond to a mechanical stimulus, activating cellular signaling pathways, ultimately resulting in gene regulation that promotes calcification of the vascular extracellular matrix (ECM). The endothelium is also thought to contribute to vascular calcification via endothelial to mesenchymal transition, creating greater cell plasticity. Each of these factors contributes to calcification, leading to increased cardiovascular mortality in patients, especially those suffering from other conditions, such as diabetes and kidney failure. Developing a better understanding of the mechanisms behind calcification may lead to the development of a potential treatment in the future.

Indexed as

BMPscadherinscanonical WNTEndMTintegrinsRUNX2smooth muscle cellsvascular calcification

Identifiers

PMID32781528
PMCPMC7552614
OpenAlexW3047593357

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.