ArticleJournal of the American Society of Nephrology : JASN2015
Circulating ADAM17 Level Reflects Disease Activity in Proteinase-3 ANCA-Associated Vasculitis.
Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- Prognostic value of miR-26b-5p in prostate cancer and its regulatory effect on tumor progression.World journal of surgical oncology · 2026Article
- Comparative phenotyping of surface markers and glycans in murine and human platelet-derived extracellular vesicles.Research and practice in thrombosis and haemostasis · 2026Article
- miR-634 Mediated Aquaporin 5 Expression Regulates the Inflammatory Response and Apoptosis in Lipopolysaccharide-Induced Human Nasal Epithelial Cells.Cell biochemistry and biophysics · 2025Article
- Neutrophils and Platelets as Key Players in the Pathogenesis of ANCA-Associated Vasculitis and Potential Sources of Disease Activity Biomarkers.Diagnostics (Basel, Switzerland) · 2025Review
- IL-6 Receptor Expression on the Surface of T Cells and Serum Soluble IL-6 Receptor Levels in Patients with Microscopic Polyangiitis and Granulomatosis with Polyangiitis.Journal of clinical medicine · 2023Article
- Genetic Predisposition to Elevated Levels of Circulating ADAM17 Is Associated with the Risk of Severe COVID-19.International journal of molecular sciences · 2023Article
- The involvement of NETs in ANCA-associated vasculitis.Frontiers in immunology · 2023Review
- TACE/ADAM17 substrates associate with ACS (Ep-CAM, HB-EGF) and follow-up MACE (TNFR1 and TNFR2).Atherosclerosis plus · 2022Article
- The Autism Spectrum Disorder-Associated Bacterial MetaboliteInternational journal of molecular sciences · 2022Article
- Analysis of microRNAs in Small Urinary Extracellular Vesicles and Their Potential Roles in Pathogenesis of Renal ANCA-Associated Vasculitis.International journal of molecular sciences · 2022Article
- The role of S100B/RAGE-enhanced ADAM17 activation in endothelial glycocalyx shedding after traumatic brain injury.Journal of neuroinflammation · 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
- B Lineage Cells in ANCA-Associated Vasculitis.International journal of molecular sciences · 2021Review
- Regulation of Platelet-Derived ADAM17: A Biomarker Approach for Breast Cancer?Diagnostics (Basel, Switzerland) · 2021Article
- Article
- Immunopathogenesis of ANCA-Associated Vasculitis.International journal of molecular sciences · 2020Review
- Degradome of soluble ADAM10 and ADAM17 metalloproteases.Cellular and molecular life sciences : CMLS · 2020Article
- Review
- B cell therapy in ANCA-associated vasculitis: current and emerging treatment options.Nature reviews. Rheumatology · 2018Review
- Pathogenetic and Clinical Aspects of Anti-Neutrophil Cytoplasmic Autoantibody-Associated Vasculitides.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ANCA-associated vasculitides are characterized by inflammatory destruction of small vessels accompanied by enhanced cleavage of membrane-bound proteins. One of the main proteases responsible for ectodomain shedding is disintegrin and metalloproteinase domain-containing protein 17 (ADAM17). Given its potential role in aggravating vascular dysfunction, we examined the role of ADAM17 in active proteinase-3 (PR3)-positive ANCA-associated vasculitis (AAV). ADAM17 concentration was significantly increased in plasma samples from patients with active PR3-AAV compared with samples from patients in remission or from other controls with renal nonvascular diseases. Comparably, plasma levels of the ADAM17 substrate syndecan-1 were significantly enhanced in active AAV. We also observed that plasma-derived ADAM17 retained its specific proteolytic activity and was partly located on extracellular microparticles. Transcript levels of ADAM17 were increased in blood samples of patients with active AAV, but those of ADAM10 or tissue inhibitor of metalloproteinases 3, which inhibits ADAMs, were not. We also performed a microRNA (miR) screen and identified miR-634 as significantly upregulated in blood samples from patients with active AAV. In vitro, miR-634 mimics induced a proinflammatory phenotype in monocyte-derived macrophages, with enhanced expression and release of ADAM17 and IL-6. These data suggest that ADAM17 has a prominent role in AAV and might account for the vascular complications associated with this disease.
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