Trial reportScientific reports2017
ADAMTS-7 is associated with a high-risk plaque phenotype in human atherosclerosis.
Trial report in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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.
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.
Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Circulating extracellular vesicles in plasma carry accessible molecular signatures of aging in mice.bioRxiv : the preprint server for biology · 2026Article
- ADAMTS-7 Increase Contributes to Worsened Neurological Outcome in Mice on High Fat Diet.CNS neuroscience & therapeutics · 2026Article
- Review
- Single cell spatial transcriptomics integration deciphers the morphological heterogeneity of atherosclerotic carotid arteries.Nature communications · 2025Article
- Genetic predisposition to immune dysregulation and extracellular matrix remodeling in cardiac arrhythmia reveals potential mediation byFrontiers in cell and developmental biology · 2025Article
- Association Between Plasma ADAMTS-7 Levels and Diastolic Dysfunction in Patients with Type 2 Diabetes Mellitus.Medicina (Kaunas, Lithuania) · 2024Article
- BAY-9835: Discovery of the First Orally Bioavailable ADAMTS7 Inhibitor.Journal of medicinal chemistry · 2024Article
- The Association ofInternational journal of molecular sciences · 2024Article
- ADAMTS-7 deficiency attenuates thoracic aortic aneurysm and dissection in mice.Journal of molecular medicine (Berlin, Germany) · 2023Article
- Article
- Molecular Mechanisms Underlying Pathological and Therapeutic Roles of Pericytes in Atherosclerosis.International journal of molecular sciences · 2022Review
- Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease.Biomedicines · 2022Review
- Article
- Genome-wide pleiotropy analysis of coronary artery disease and pneumonia identifies shared immune pathways.Science advances · 2022Article
- TAILS Identifies Candidate Substrates and Biomarkers of ADAMTS7, a Therapeutic Protease Target in Coronary Artery Disease.Molecular & cellular proteomics : MCP · 2022Article
- ADAM and ADAMTS disintegrin and metalloproteinases as major factors and molecular targets in vascular malfunction and disease.Advances in pharmacology (San Diego, Calif.) · 2022Article
- Development of a fluorogenic ADAMTS-7 substrate.Journal of enzyme inhibition and medicinal chemistry · 2021Article
- Coronary Disease Association With ADAMTS7 Is Due to Protease Activity.Circulation research · 2021Article
- ADAMTS proteases and the tumor immune microenvironment: Lessons from substrates and pathologies.Matrix biology plus · 2021Review
- ADAMTS proteases in cardiovascular physiology and disease.Open biology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several large-scale genome-wide association studies have identified single-nucleotide polymorphisms in the genomic region of A Disintegrin And Metalloproteinase with ThromboSpondin type 1 repeats (ADAMTS)-7 and associations to coronary artery disease. Experimental studies have provided evidence for a functional role of ADAMTS-7 in both injury-induced vascular neointima formation and development of atherosclerotic lesions. However, whether ADAMTS-7 is associated with a specific plaque phenotype in humans has not been investigated. Carotid plaques (n = 206) from patients with and without cerebrovascular symptoms were analyzed for expression of ADAMTS-7 by immunohistochemistry and correlated to components associated with plaque vulnerability. Plaques from symptomatic patients showed increased levels of ADAMTS-7 compared with lesions from asymptomatic patients. High levels of ADAMTS-7 correlated with high levels of CD68-staining and lipid content, but with low smooth muscle cell and collagen content, which together are characteristics of a vulnerable plaque phenotype. ADAMTS-7 levels above median were associated with increased risk for postoperative cardiovascular events. Our data show that ADAMTS-7 is associated with a vulnerable plaque phenotype in human carotid lesions. These data support previous observations of a potential proatherogenic role of ADAMTS-7.
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What OpenQuestion holds
Registered trials
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.