Evidence map›Paper›PMID 32166823›Full record

ReviewPathology international2020

Pathophysiology of atherothrombosis: Mechanisms of thrombus formation on disrupted atherosclerotic plaques.

Yujiro Asada, Atsushi Yamashita, Yuichiro Sato, Kinta Hatakeyama

Open access · hybridAbstract readReview
In one paragraph

Review in Pathology international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 1 pooled it
9.0field-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

76 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  8. Review
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  12. Article
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  16. Article
  17. Spatial Myeloid Landscape of Large Artery Atherosclerotic and Cardioembolic Thrombi Retrieved by Mechanical Thrombectomy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  18. Gout, Uric Acid, and Coronary Artery Disease.Journal of atherosclerosis and thrombosis · 2025
    Review
  19. Review
  20. Article

16 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

4 authors at 3 institutions in 1 country.

Yujiro AsadaPathophysiology Section, Department of Pathology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Atsushi YamashitaPathophysiology Section, Department of Pathology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.ORCID http://orcid.org/0000-0001-5487-7594
Yuichiro SatoDepartment of Diagnostic Pathology, University of Miyazaki Hospital, University of Miyazaki, Miyazaki, Japan.
Kinta HatakeyamaDepartment of Diagnostic Pathology, Nara Medical University, Nara, Japan.
University of Miyazaki · JPNara Medical University · JPUniversity of Miyazaki Hospital · JP

Funding

Japan Society for the Promotion of Science 16H05163Japan Society for the Promotion of Science 19H03445Japan Society for the Promotion of Science 20390102Japan Society for the Promotion of Science 23390084National Cerebral and Cardiovascular Center 25-4-3
6 · The paper itself

Abstract

Atherothrombosis is a leading cause of cardiovascular mortality and morbidity worldwide. The underlying mechanisms of atherothrombosis comprise plaque disruption and subsequent thrombus formation. Arterial thrombi are thought to mainly comprise aggregated platelets as a result of high blood velocity. However, thrombi that develop on disrupted plaques comprise not only aggregated platelets, but also large amounts of fibrin, because plaques contain large amount of tissue factor that activate the coagulation cascade. Since not all thrombi grow large enough to occlude the vascular lumen, the propagation of thrombi is also critical in the onset of adverse vascular events. Various factors such as vascular wall thrombogenicity, local hemorheology, systemic thrombogenicity and fibrinolytic activity modulate thrombus formation and propagation. Although the activation mechanisms of platelets and the coagulation cascade have been intensively investigated, the underlying mechanisms of occlusive thrombus formation on disrupted plaques remain obscure. Pathological findings derived from humans and animal models of human atherothrombosis have uncovered pathophysiological processes during thrombus formation and propagation after plaque disruption, and novel factors have been identified that modulate the activation of platelets and the coagulation cascade. These findings have also provided insights into the development of novel drugs for atherothrombosis.

Indexed as

AnimalsAtherosclerosisHumansThrombosisatherothrombosisblood flowcoagulation factorplateletvasoconstriction

Identifiers

PMID32166823
PMCPMC7317428
OpenAlexW3012021885

What Socratic holds

Textmetadata
LicenceCC BY-NC
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.