ArticleNature medicine2017
Nitric oxide mediates aortic disease in mice deficient in the metalloprotease Adamts1 and in a mouse model of Marfan syndrome.
Article in Nature medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
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Who cites it
114 citing papers in PubMed, 174 citations in OpenAlex.
- Regulation of PDE5 expression in human aorta and thoracic aortic aneurysms.Scientific reports · 2019Trial
- The aorta in Marfan syndrome: from molecular mechanisms to mechanobiological dysfunction.Cardiovascular research · 2026Review
- Genetic and molecular mechanisms of hereditary thoracic aortic aneurysm and dissection (Review).Molecular medicine reports · 2026Review
- Fibronectin-induced overactivation of αNature communications · 2026Article
- Mechanotransduction in Marfan Syndrome and Related Aortic Disorders: Insights from Transcriptomic Analyses.Genes · 2026Review
- Chromobox 3 assembles an epigenetic complex contributing to cystathionine γ-lyase-mediated protection against aortic aneurysm/dissection.Nature communications · 2026Article
- The Dual Role of ADAMTS1 in Cardiovascular Remodeling: Balancing Extracellular Matrix Homeostasis and Pathological States.Journal of cardiovascular development and disease · 2025Review
- Obesity: An Underlying Risk for Acute Aortic Dissection.Journal of clinical medicine · 2025Review
- The Pathophysiological Role of Vascular Smooth Muscle Cells in Abdominal Aortic Aneurysm.Cells · 2025Review
- Article
- Endothelial Cell Senescence in Marfan Syndrome: Pathogenesis and Therapeutic Potential of TGF-β Pathway Inhibition.Journal of the American Heart Association · 2025Article
- Recommendations for Design, Execution, and Reporting of Studies on Experimental Thoracic Aortopathy in Preclinical Models.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- Phosphatase-independent activity of smooth-muscle calcineurin orchestrates a gene expression program leading to hypertension.PLoS biology · 2025Article
- Adamts1 and Cyst Expansion in Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2025Article
- The TRPM7 chanzyme in smooth muscle cells drives abdominal aortic aneurysm in mice.Nature cardiovascular research · 2025Article
- Inhibition of aortic CX3CR1+ macrophages mitigates thoracic aortic aneurysm progression in Marfan syndrome in mice.The Journal of clinical investigation · 2025Article
- Fibrillin-1 Deficiency Perturbs Aortic Cholinergic Relaxation and Adrenergic Contraction in a Mouse Model of Early Onset Progressively Severe Marfan Syndrome.Journal of vascular research · 2025Article
- Association Between Lipoprotein(a) and Dilatation of Different Aortic Segments in Hypertensive Patients.Echocardiography (Mount Kisco, N.Y.) · 2025Article
- Therapeutic Opportunities of Marfan Syndrome: Current Perspectives.Drug design, development and therapy · 2025Review
- Genetic Manipulation of Caveolin-1 in a Transgenic Mouse Model of Aortic Root Aneurysm: Sex-Dependent Effects on Endothelial and Smooth Muscle Function.International journal of molecular sciences · 2024Article
54 more citing papers are in PubMed but not listed here.
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Authors and funding
18 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heritable thoracic aortic aneurysms and dissections (TAAD), including Marfan syndrome (MFS), currently lack a cure, and causative mutations have been identified for only a fraction of affected families. Here we identify the metalloproteinase ADAMTS1 and inducible nitric oxide synthase (NOS2) as therapeutic targets in individuals with TAAD. We show that Adamts1 is a major mediator of vascular homeostasis, given that genetic haploinsufficiency of Adamts1 in mice causes TAAD similar to MFS. Aortic nitric oxide and Nos2 levels were higher in Adamts1-deficient mice and in a mouse model of MFS (hereafter referred to as MFS mice), and Nos2 inactivation protected both types of mice from aortic pathology. Pharmacological inhibition of Nos2 rapidly reversed aortic dilation and medial degeneration in young Adamts1-deficient mice and in young or old MFS mice. Patients with MFS showed elevated NOS2 and decreased ADAMTS1 protein levels in the aorta. These findings uncover a possible causative role for the ADAMTS1-NOS2 axis in human TAAD and warrant evaluation of NOS2 inhibitors for therapy.
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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 Socratic graph.