Evidence map›Paper›PMID 30349892›Full record

ArticleResearch and practice in thrombosis and haemostasis2018

Indoleamine 2,3-dioxygenase 1 in coronary atherosclerotic plaque enhances tissue factor expression in activated macrophages.

Yuki Watanabe, Shohei Koyama, Atsushi Yamashita, Yunosuke Matsuura, Kensaku Nishihira, Kazuo Kitamura, Yujiro Asada

Open access · goldAbstract read
In one paragraph

Article in Research and practice in thrombosis and haemostasis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

26 citing papers in PubMed, 35 citations in OpenAlex.

  1. Foods (Basel, Switzerland) · 2026
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  7. Mechanisms of metabolic reprogramming in abdominal aortic aneurysm.Frontiers in cell and developmental biology · 2025
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  18. The Footprint of Kynurenine Pathway in Cardiovascular Diseases.International journal of tryptophan research : IJTR · 2022
    Review
  19. Article
  20. Review
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

7 authors at 1 institution in 1 country.

Yuki WatanabeDepartment of Pathology Faculty of Medicine University of Miyazaki Miyazaki Japan.
Shohei KoyamaDepartment of Pathology Faculty of Medicine University of Miyazaki Miyazaki Japan.
Atsushi YamashitaDepartment of Pathology Faculty of Medicine University of Miyazaki Miyazaki Japan.
Yunosuke MatsuuraDepartment of Internal Medicine Faculty of Medicine University of Miyazaki Miyazaki Japan.
Kensaku NishihiraDepartment of Internal Medicine Faculty of Medicine University of Miyazaki Miyazaki Japan.
Kazuo KitamuraDepartment of Internal Medicine Faculty of Medicine University of Miyazaki Miyazaki Japan.
Yujiro AsadaDepartment of Pathology Faculty of Medicine University of Miyazaki Miyazaki Japan.
University of Miyazaki · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent clinical studies have found that changes in the kynurenine (Kyn) pathway of tryptophan (Trp) metabolism are associated with cardiovascular events. However, the roles of the Kyn pathway on vascular wall thrombogenicity remain unknown. Indoleamine 2,3-dioxygenase 1 (IDO1) is a rate-limiting enzyme of the Kyn pathway.

objectiveThe present study aimed to localize IDO1 in human coronary atherosclerotic plaques from patients with angina pectoris and define its role in plaque thrombogenicity.

methodsImmunohistochemical methods were applied to localize IDO1 in coronary atherosclerotic plaques from patients with stable (SAP) and unstable (UAP) angina pectoris. The role of IDO1 in tissue factor (TF) expression was investigated in THP-1 macrophages activated by interferon (IFN)γ and tissue necrosis factor (TNF)α.

resultsWe localized IDO1 mainly in CD68-positive macrophages within atherosclerotic plaques, and in close association with TF. Areas that were immunopositive for IDO1, TF, and CD3-positive T lymphocytes were significantly larger in plaques from patients with UAP than SAP. Macrophages activated by IFNγ and TNFα upregulated IDO1 expression, increased the Kyn/Trp ratio and enhanced TF expression and activity, but not TF pathway inhibitor expression. The IDO1 inhibitor epacadostat significantly reduced the Kyn/Trp ratio, TF expression and activity, as well as NF-κB (p65) binding activity in activated macrophages. Inhibition of the aryl hydrocarbon receptor that binds to Kyn, also reduced Kyn-induced TF expression in activated macrophages.

conclusionIndoleamine 2,3-dioxygenase 1 expressed in coronary atherosclerotic plaques might contribute to thrombus formation through TF upregulation in activated macrophages.

Indexed as

aryl hydrocarbon receptorindoleamin 2,3‐dioxygenase 1macrophagethrombosistissue factor

Identifiers

PMID30349892
PMCPMC6178752
OpenAlexW2883491095

What OpenQuestion holds

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Registered trials

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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.