Evidence map›Paper›PMID 40115634›Full record

ArticleJournal of molecular and cellular cardiology plus2025

ADAMTS7, a target in atherosclerosis, cooperates with its homolog ADAMTS12 to protect against myxomatous valve degeneration.

Timothy J Mead, Sumit Bhutada, Niccolò Peruzzi, Janet Adegboye, Deborah E Seifert, Elisabeth Cahill, Jeanne Drinko, Eoin Donnellan, Anu Guggiliam, Zoran Popovic and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of molecular and cellular cardiology plus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. An Overview of ADAMTS Proteases.Methods in molecular biology (Clifton, N.J.) · 2026
    Review
  7. Article
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

13 authors.

Timothy J MeadDepartment of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
Sumit BhutadaDepartment of Biomedical Engineering, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA.
Niccolò PeruzziDepartment of Experimental Medical Science and Wallenberg Center for Molecular Medicine, Lund University, Lund, Sweden.
Janet AdegboyeDepartment of Biomedical Engineering, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA.
Deborah E SeifertDepartment of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
Elisabeth CahillDepartment of Biomedical Engineering, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA.
Jeanne DrinkoDepartment of Cardiovascular Medicine, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA.
Eoin DonnellanDepartment of Cardiovascular Medicine, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA.
Anu GuggiliamDepartment of Cellular and Molecular Medicine, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA.
Zoran PopovicDepartment of Cardiovascular Medicine, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA.
Brian GriffinDepartment of Cardiovascular Medicine, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA.
Karin Tran-LundmarkDepartment of Experimental Medical Science and Wallenberg Center for Molecular Medicine, Lund University, Lund, Sweden.
Suneel S ApteDepartment of Biomedical Engineering, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA.

Funding

Impact of microfibril turnover on vascular development and diseaseR01HL156987 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI Timothy Joseph Mead · 2022 to 2026
$2.0M
NHLBI NIH HHS R01 HL156987
6 · The paper itself

Abstract

The physiological roles of the metalloprotease-proteoglycan ADAMTS7, a drug target in atherosclerosis and vascular restenosis, and its homolog ADAMTS12, are undefined in the cardiovascular system. The objective of the present work was to investigate their roles in mice with genetic inactivation of both proteases and in relation to the resulting valve defects, to define their proteolytic activities in the matrisome. Here, we demonstrate that

Indexed as

ADAMTSExtracellular matrixFibrosisHeart valveHypertrophyMetalloproteinaseMyxomatous valveProteoglycanRegurgitation

Identifiers

PMID40115634
PMCPMC11925103

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.