ArticleScientific reports2016
Loss of ADAMTS4 reduces high fat diet-induced atherosclerosis and enhances plaque stability in ApoE(-/-) mice.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 56 citations in OpenAlex.
- The matrix proteins aggrecan and fibulin-1 play a key role in determining aortic stiffness.Scientific reports · 2018Trial
- ADAMTS-7 Increase Contributes to Worsened Neurological Outcome in Mice on High Fat Diet.CNS neuroscience & therapeutics · 2026Article
- Exploring the Role of ADAMTS4 Expression in Atherosclerosis.Methods in molecular biology (Clifton, N.J.) · 2026Article
- ADAMTS4-Specific MR Peptide Probe for the Assessment of Atherosclerotic Plaque Burden in a Mouse Model.Investigative radiology · 2025Article
- ADAMTS4 Reduction Contributes to Extracellular Matrix Deposition and Impaired Myogenesis in the Skeletal Muscle of Cigarette Smoke-Exposed Mice.Biomedicines · 2025Article
- Overexpression of Neural Precursor Cell Expressed Developmentally Downregulated 9 (NEDD9) reduces ox-LDL-induced Anoikis in atherosclerotic vascular endothelial cells.International journal of cardiology. Heart & vasculature · 2025Article
- Inhibition of the extracellular enzyme A disintegrin and metalloprotease with thrombospondin motif 4 prevents cardiac fibrosis and dysfunction.Cardiovascular research · 2023Article
- ADAMTS7: a Novel Therapeutic Target in Atherosclerosis.Current atherosclerosis reports · 2023Review
- Restoration of normal blood flow in atherosclerotic arteries promotes plaque stabilization.iScience · 2023Article
- A novel interleukin-2-based fusion molecule, HCW9302, differentially promotes regulatory T cell expansion to treat atherosclerosis in mice.Frontiers in immunology · 2023Article
- Estrogen Receptor Subtypes Elicit a Distinct Gene Expression Profile of Endothelial-Derived Factors Implicated in Atherosclerotic Plaque Vulnerability.International journal of molecular sciences · 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
- Novel Nongenetic Murine Model of Hyperglycemia and Hyperlipidemia-Associated Aggravated Atherosclerosis.Frontiers in cardiovascular medicine · 2022Article
- Hyalectanase Activities by the ADAMTS Metalloproteases.International journal of molecular sciences · 2021Review
- ADAMTS proteases and the tumor immune microenvironment: Lessons from substrates and pathologies.Matrix biology plus · 2021Review
- Atherosclerosis Pathways are Activated in Pericoronary Adipose Tissue of Patients with Coronary Artery Disease.Journal of inflammation research · 2021Article
- High-Throughput Screening of Mouse Gene Knockouts Identifies Established and Novel High Body Fat Phenotypes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- Statins Mitigate Stress-Related Vascular Aging and Atherosclerosis inFrontiers in cell and developmental biology · 2021Article
- ADAMTS proteases in cardiovascular physiology and disease.Open biology · 2020Review
- The Effects of Pro-Inflammatory and Anti-Inflammatory Agents for the Suppression of Intimal Hyperplasia: An Evidence-Based Review.International journal of environmental research and public health · 2020Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis is a chronic inflammatory disease characterized by formation of lipid-rich plaques on the inner walls of arteries. ADAMTS4 (a disintegrin-like and metalloproteinase with thrombospondin motifs-4) is a secreted proteinase that regulates versican turnover in the arterial wall and atherosclerotic plaques. Recent reports indicated elevated ADAMTS4 level in human atherosclerotic plaques and in the plasma of acute coronary syndrome patients. Nevertheless, whether increased ADAMTS4 is a consequence of atherosclerosis or ADAMTS4 has a causal role in atherogenesis remains unknown. In this work, we investigated the role of ADAMTS4 in diet induced atherosclerosis using apolipoprotein E deficient (ApoE(-/-)) and Adamts4 knockout mice. We show that ADAMTS4 expression increases in plaques as atherosclerosis progresses in ApoE(-/-) mice. ApoE(-/-)Adamts4(-/-) double knockout mice presented a significant reduction in plaque burden at 18 weeks of age. Loss of ADAMTS4 lead to a more stable plaque phenotype with a significantly reduced plaque vulnerability index characterized by reduced lipid content and macrophages accompanied with a significant increase in smooth muscle cells, collagen deposition and fibrotic cap thickness. The reduced atherosclerosis is accompanied by an altered plasma inflammatory cytokine profile. These results demonstrate for the first time that ADAMTS4 contributes to diet induced atherosclerosis in ApoE(-/-) mice.
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