Evidence map›Paper›PMID 30727754›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2019

Osteopontin in Vascular Disease.

Zoe Shin Yee Lok, Alicia N Lyle

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed
18.0field-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

130 citing papers in PubMed, 200 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. SPP1BMC medicine · 2026
    Article
  5. Article
  6. Review
  7. Comparative Investigation of the Effects of Entelon150Journal of clinical medicine · 2026
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Transcriptome Analysis IdentifiedJournal of the American Heart Association · 2025
    Article
  19. Characterizing Stroke Clots Using Single-Cell Sequencing.Journal of the American Heart Association · 2025
    Article
  20. Paeonol fromFood science and biotechnology · 2025
    Article

70 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 1 institution in 1 country.

Zoe Shin Yee LokDepartment of Surgery, School of Clinical Sciences, Monash Health, Clayton, Australia (Z.S.Y.L.).
Alicia N LyleFrom the Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA (A.N.L.).
Emory University · US

Funding

Implementing a Maternal health and PRegnancy Outcomes Vision for Everyone (IMPROVE)UL1TR002378 · NCATS · EMORY UNIVERSITY · PI Andres J Garcia, Elizabeth O. Ofili · 2017 to 2026
$92.1M
The Role of Human Osteopontin Isoforms in Collateral FormationR00HL119567 · NHLBI · EMORY UNIVERSITY · PI LYLE, ALICIA N · 2015 to 2017
$732k
The Role of Human Osteopontin Isoforms in Collateral FormationK99HL119567 · NHLBI · EMORY UNIVERSITY · PI LYLE, ALICIA N · 2014 to 2015
$197k
NCATS NIH HHS UL1 TR002378NHLBI NIH HHS K99 HL119567NHLBI NIH HHS R00 HL119567
6 · The paper itself

Abstract

Inflammatory cytokines are necessary for an acute response to injury and the progressive healing process. However, when this acute response does not resolve and becomes chronic, the same proteins that once promoted healing then contribute to chronic inflammatory pathologies, such as atherosclerosis. OPN (Osteopontin) is a secreted matricellular cytokine that signals through integrin and CD44 receptors, is highly upregulated in acute and chronic inflammatory settings, and has been implicated in physiological and pathophysiologic processes. Evidence from the literature suggests that OPN may fit within the Goldilocks paradigm with respect to cardiovascular disease, where acute increases are protective, attenuate vascular calcification, and promote postischemic neovascularization. In contrast, chronic increases in OPN are clinically associated with an increased risk for a major adverse cardiovascular event, and OPN expression is a strong predictor of cardiovascular disease independent of traditional risk factors. With the recent finding that humans express multiple OPN isoforms as the result of alternative splicing and that these isoforms have distinct biologic functions, future studies are required to determine what OPN isoform(s) are expressed in the setting of vascular disease and what role each of these isoforms plays in vascular disease progression. This review aims to discuss our current understanding of the role(s) of OPN in vascular disease pathologies using evidence from in vitro, animal, and clinical studies. Where possible, we discuss what is known about OPN isoform expression and our understanding of OPN isoform contributions to cardiovascular disease pathologies.

Indexed as

Alternative SplicingAnimalsAtherosclerosisCalcinosisGlycosylationHumansHyaluronan ReceptorsInflammationIntegrinsIschemiaMiceModels, CardiovascularNeointimaOsteopontinPhosphorylationProtein IsoformsCD44 protein, humanHyaluronan ReceptorsIntegrinsOsteopontinProtein IsoformsSPP1 protein, humanatherosclerosiscytokinesinflammationosteopontinrisk factorsvascular diseases

Identifiers

PMID30727754
PMCPMC6436981
OpenAlexW2921614510

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.