Evidence map›Paper›PMID 37547071›Full record

ArticleJACC. Basic to translational science2023

Bioprosthetic Valve Deterioration: Accumulation of Circulating Proteins and Macrophages in the Valve Interstitium.

Tomohisa Sakaue, Tadaaki Koyama, Yoshitsugu Nakamura, Keitaro Okamoto, Takayuki Kawashima, Tadashi Umeno, Yasuhide Nakayama, Shinji Miyamoto, Fumiaki Shikata, Mika Hamaguchi and 8 more

Abstract read
In one paragraph

Article in JACC. Basic to translational science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Review
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  7. Article
  8. Macrophages as key modulators of calcific aortic valve disease.Frontiers in cardiovascular medicine · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
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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

18 authors.

Tomohisa SakaueDepartment of Cardiovascular and Thoracic Surgery, Ehime University Graduate School of Medicine, Toon, Japan.
Tadaaki KoyamaDepartment of Cardiovascular Surgery, Kobe City Medical Center General Hospital, Kobe, Japan.
Yoshitsugu NakamuraDepartment of Cardiovascular Surgery, Chiba-Nishi General Hospital, Matsudo, Japan.
Keitaro OkamotoDepartment of Cardiovascular Surgery, Oita University, Yufu, Japan.
Takayuki KawashimaDepartment of Cardiovascular Surgery, Oita University, Yufu, Japan.
Tadashi UmenoDepartment of Cardiovascular Surgery, Oita University, Yufu, Japan.
Yasuhide NakayamaDepartment of Cardiovascular Surgery, Oita University, Yufu, Japan.
Shinji MiyamotoDepartment of Cardiovascular Surgery, Oita University, Yufu, Japan.
Fumiaki ShikataDepartment of Cardiovascular and Thoracic Surgery, Ehime University Graduate School of Medicine, Toon, Japan.
Mika HamaguchiDepartment of Cardiology, Pulmonology, Hypertension, and Nephrology, Ehime University Graduate School of Medicine, Toon, Japan.
Jun AonoDepartment of Cardiology, Pulmonology, Hypertension, and Nephrology, Ehime University Graduate School of Medicine, Toon, Japan.
Mie KurataDepartment of Pathology, Division of Analytical Pathology, Ehime University Graduate School of Medicine, Toom, Japan.
Kenji NamiguchiDepartment of Cardiovascular and Thoracic Surgery, Ehime University Graduate School of Medicine, Toon, Japan.
Shunji UchitaDepartment of Cardiovascular and Thoracic Surgery, Ehime University Graduate School of Medicine, Toon, Japan.
Junya MasumotoDepartment of Pathology, Division of Analytical Pathology, Ehime University Graduate School of Medicine, Toom, Japan.
Osamu YamaguchiDepartment of Cardiology, Pulmonology, Hypertension, and Nephrology, Ehime University Graduate School of Medicine, Toon, Japan.
Shigeki HigashiyamaDepartment of Cell Growth and Tumor Regulation, Proteo-Science Center, Toon, Japan.
Hironori IzutaniDepartment of Cardiovascular and Thoracic Surgery, Ehime University Graduate School of Medicine, Toon, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histologic evaluations revealed excessive accumulations of macrophages and absence of fibroblastic interstitial cells in explanted bioprosthetic valves. Comprehensive gene and protein expression analysis and histology unveiled an accumulation of fibrinogen and plasminogen, an activator of infiltrated macrophages, from degenerated valve surfaces in the interstitial spaces. These pathologies were completely reproduced in a goat model replaced with an autologous pericardium-derived aortic valve. Further preclinical animal experiments using goats demonstrated that preventing infiltration of macrophages and circulating proteins by increasing collagen density and leaflet strength is an effective treatment option.

Indexed as

bioprosthetic valvecalcificationmacrophageplasma proteinstructural valve deterioration

Identifiers

PMID37547071
PMCPMC10401294

What OpenQuestion holds

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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.