ReviewMediators of inflammation2015
The Function and Roles of ADAMTS-7 in Inflammatory Diseases.
Review in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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
18 citing papers in PubMed, 30 citations in OpenAlex.
- Current Advances in the Physiological Roles and Disease-Associated Mechanisms of ADAMTS16.International journal of molecular sciences · 2026Review
- ADAMTS-7 Increase Contributes to Worsened Neurological Outcome in Mice on High Fat Diet.CNS neuroscience & therapeutics · 2026Article
- Review
- Article
- ADAMTS7 promotes smooth muscle foam cell expansion in atherosclerosis.The Journal of clinical investigation · 2026Article
- ADAMTS5 May Serve as a Useful Biomarker for Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2026Article
- Degenerating intervertebral discs in the streptozotocin-high-fat diet model of type 2 diabetes show extensive inflammation.Disease models & mechanisms · 2025Article
- The transcriptome and secreted factors of the intervertebral discs in STZ-HFD Type 2 diabetic male mice reveal extensive inflammation.bioRxiv : the preprint server for biology · 2025Article
- Associations of SEMA7A, SEMA4D, ADAMTS10, and ADAM8 with KRAS, NRAS, BRAF, PIK3CA, and AKT Gene Mutations, Microsatellite Instability Status, and Cytokine Expression in Colorectal Cancer Tissue.Current issues in molecular biology · 2024Article
- Article
- Epigenetic regulatory mechanism of ADAMTS12 expression in osteoarthritis.Molecular medicine (Cambridge, Mass.) · 2023Article
- The Mechanism and Role of ADAMTS Protein Family in Osteoarthritis.Biomolecules · 2022Review
- Cartilage Targets of Knee Osteoarthritis Shared by Both Genders.International journal of molecular sciences · 2021Article
- Article
- Inhibition of MMPs and ADAM/ADAMTS.Biochemical pharmacology · 2019Review
- Wnt and RUNX2 mediate cartilage breakdown by osteoarthritis synovial fibroblast-derived ADAMTS-7 and -12.Journal of cellular and molecular medicine · 2019Article
- Nobiletin Inhibits IL-1β-Induced Inflammation in ChondrocytesFrontiers in pharmacology · 2019Article
- Association of coronary artery disease related single nucleotide-polymorphisms with extreme Prakriti types: Insights from a case control study.Journal of Ayurveda and integrative medicineArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ADAMTS proteinases are a group of multidomain and secreted metalloproteinases containing the thrombospondin motifs. ADAMTS-7 is a member of ADAMTS family and plays a crucial role in the pathogenesis of arthritis. Overexpression of ADAMTS-7 gene promotes the breakdown of cartilage oligomeric matrix protein (COMP) matrix and accelerates the progression of both surgically induced osteoarthritis and collagen-induced arthritis. Moreover, ADAMTS-7 and tumor necrosis factor-α (TNF-α) form a positive feedback loop in osteoarthritis. More significantly, granulin-epithelin precursor, a growth factor has important roles in bone development and bone-associated diseases, disturbs the interaction between ADAMTS-7 and COMP, and prevents COMP degradation. This review is based on our results and provides an overview of current knowledge of ADAMTS-7, including its structure, function, gene regulation, and inflammatory diseases involvement.
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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.