Evidence map›Paper›PMID 40429650›Full record

ArticleInternational journal of molecular sciences2025

Exploring the Histopathological Features of Thrombus-Associated Localized Amyloid Deposition: Comprehensive Analysis Employing Immunohistochemistry and Proteomics.

Shojiro Ichimata, Tsuneaki Yoshinaga, Mitsuto Sato, Nagaaki Katoh, Fuyuki Kametani, Masahide Yazaki, Yoshiki Sekijim, Yukiko Hata, Naoki Nishida

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Shojiro IchimataDepartment of Legal Medicine, Faculty of Medicine, University of Toyama, Toyama 930-0194, Japan.ORCID 0000-0002-7305-8137
Tsuneaki YoshinagaDepartment of Medicine (Neurology and Rheumatology), Shinshu University School of Medicine, Matsumoto 390-8621, Japan.ORCID 0000-0002-4323-0557
Mitsuto SatoDepartment of Medicine (Neurology and Rheumatology), Shinshu University School of Medicine, Matsumoto 390-8621, Japan.
Nagaaki KatohDepartment of Medicine (Neurology and Rheumatology), Shinshu University School of Medicine, Matsumoto 390-8621, Japan.
Fuyuki KametaniDepartment of Brain and Neurosciences, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.ORCID 0000-0001-9125-7001
Masahide YazakiClinical Laboratory Sciences Division, Shinshu University Graduate School of Medicine, Shinshu University, Matsumoto 390-8621, Japan.ORCID 0000-0001-5520-6530
Yoshiki SekijimDepartment of Medicine (Neurology and Rheumatology), Shinshu University School of Medicine, Matsumoto 390-8621, Japan.
Yukiko HataDepartment of Legal Medicine, Faculty of Medicine, University of Toyama, Toyama 930-0194, Japan.
Naoki NishidaDepartment of Legal Medicine, Faculty of Medicine, University of Toyama, Toyama 930-0194, Japan.ORCID 0000-0002-6921-1768

Funding

Japan Society for the Promotion of Science JP20K18979
6 · The paper itself

Abstract

Amyloid deposition has been reported to localize within thrombi; however, its pathological characteristics, particularly its precursor proteins, remain poorly understood. This study aimed to elucidate the pathological features of thrombus-associated amyloid deposition by immunohistochemistry combined with proteomic analyses using liquid chromatography-tandem mass spectrometry with laser microdissection. Our findings revealed that thrombus-associated amyloid deposits within the thrombus and vessel wall primarily comprised apolipoprotein A-I, with a mixture of amyloid fibrils derived from amyloidogenic proteins, including transthyretin and lactoferrin. Given that these proteins are present in the blood, our results support a previous hypothesis that proteins denatured during thrombus aging are a source of amyloid. Furthermore, phagocytes were infiltrated around the intramural and extravascular deposits rather than around the amyloid deposits within the thrombus. Therefore, amyloid deposits generated within the thrombus may be transported from regions with limited blood flow to the vessel wall and surrounding tissues, where blood flow is present, during thrombus processing. These deposits were primarily removed by phagocytic cells. Our results suggest that a facilitative effect on deposition occurs via a cross-seeding mechanism between amyloid fibrils and that phagocytes can remove amyloid deposits. These findings help elucidate the pathogenesis of localized amyloidosis.

Indexed as

AmyloidAmyloidosisProteomicsThrombosisAgedFemaleHumansImmunohistochemistryLactoferrinMaleMiddle AgedPhagocytesPrealbuminTandem Mass SpectrometryAmyloidLactoferrinPrealbuminapolipoprotein A-Iatherosclerosislactoferrinlocalized amyloidosisphagocyteproteomicsthrombustransthyretin

Identifiers

PMID40429650
PMCPMC12111168

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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.