ArticlePloS one2017
ADAMTS-1 in abdominal aortic aneurysm.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- The Dual Role of ADAMTS1 in Cardiovascular Remodeling: Balancing Extracellular Matrix Homeostasis and Pathological States.Journal of cardiovascular development and disease · 2025Review
- ADAMTS4-Specific MR Peptide Probe for the Assessment of Atherosclerotic Plaque Burden in a Mouse Model.Investigative radiology · 2025Article
- Review
- Emerging roles for the ADAMTS-like family of matricellular proteins in cardiovascular disease through regulation of the extracellular microenvironment.Molecular biology reports · 2024Review
- Disintegrin and Metalloproteinases (ADAMs [A Disintegrin and Metalloproteinase] and ADAMTSs [ADAMs With a Thrombospondin Motif]) in Aortic Aneurysm.Hypertension (Dallas, Tex. : 1979) · 2022Review
- ADAM and ADAMTS disintegrin and metalloproteinases as major factors and molecular targets in vascular malfunction and disease.Advances in pharmacology (San Diego, Calif.) · 2022Article
- KLF11 protects against abdominal aortic aneurysm through inhibition of endothelial cell dysfunction.JCI insight · 2021Article
- Targeting the Extracellular Matrix in Abdominal Aortic Aneurysms Using Molecular Imaging Insights.International journal of molecular sciences · 2021Review
- Aortic Dilatation in Patients With Bicuspid Aortic Valve.Frontiers in physiology · 2021Review
- ADAM (a Disintegrin and Metalloproteinase) 15 Deficiency Exacerbates Ang II (Angiotensin II)-Induced Aortic Remodeling Leading to Abdominal Aortic Aneurysm.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- MMPs and ADAMs/ADAMTS inhibition therapy of abdominal aortic aneurysm.Life sciences · 2020Review
- MiR-126a-5p limits the formation of abdominal aortic aneurysm in mice and decreases ADAMTS-4 expression.Journal of cellular and molecular medicine · 2020Article
- Pathogenic mechanisms and the potential of drug therapies for aortic aneurysm.American journal of physiology. Heart and circulatory physiology · 2020Review
- Altered IL-32 Signaling in Abdominal Aortic Aneurysm.Journal of vascular research · 2020Article
- Extracellular matrix, regional heterogeneity of the aorta, and aortic aneurysm.Experimental & molecular medicine · 2019Review
- miR-365b-3p inhibits the cell proliferation and migration of human coronary artery smooth muscle cells by directly targeting ADAMTS1 in coronary atherosclerosis.Experimental and therapeutic medicine · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionExtracellular matrix degradation is a hallmark of abdominal aortic aneurysm (AAA). Among proteases that are capable of degrading extracellular matrix are a disintegrin and metalloproteases with thrombospondin motifs (ADAMTS). Pathogenesis of these proteases in AAA has not been investigated until date. METHODS AND
resultsHuman aneurysmal and control aortas were collected and analyzed with RT-PCR measuring the ADAMTS-1, 4,5,6,8,9,10,13,17 and ADAMTSL-1. Expression of a majority of the investigated ADAMTS members on mRNA level was decreased in aneurysm compared to control aorta. ADAMTS-1 was one of the members that was reduced most. Protein analysis using immunohistochemistry and western blot for localization and expression of ADAMTS-1 revealed that ADAMTS-1 was present predominantly in areas of SMCs and macrophages in aneurysmal aorta and higher expressed in AAA compared to control aortas. The role of ADAMTS-1 in AAA disease was further examined using ADAMTS-1 transgenic/apoE-/- mice with the experimental angiotensin II induced aneurysmal model. Transgenic mice overexpressing ADAMTS-1 showed to be similar to ADAMTS-1 wild type mice pertaining collagen, elastin content and aortic diameter.
conclusionSeveral of the ADAMTS members, and especially ADAMTS-1, are down regulated at mRNA level in AAA, due to unknown mechanisms, at the same time ADAMTS-1 protein is induced. The cleavage of its substrates, don't seem to be crucial for the pathogenesis of AAA but rather more important in the development of thoracic aortic aneurysm and atherosclerosis as shown in previous studies.
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