ArticleThe Annals of thoracic surgery2017
A Novel Murine Model of Marfan Syndrome Accelerates Aortopathy and Cardiomyopathy.
Article in The Annals of thoracic surgery, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Hypertension drives thoracic aortic aneurysm and dissection in male, but not female, Marfan mice.Journal of the mechanical behavior of biomedical materials · 2026Article
- Angiotensin II Induces Abdominal Aortic Branch Aneurysms inArteriosclerosis, thrombosis, and vascular biology · 2026Article
- Structural and Signaling Mechanisms of Aortic Wall Failure in Heritable Thoracic Aortic Disease.Cells · 2026Review
- Systematic Disruption of Zebrafish Fibrillin Genes Identifies a Translational Zebrafish Model for Marfan Syndrome.JACC. Basic to translational science · 2026Article
- Intrinsic cardiomyopathy in pediatric Marfan syndrome: predictive factors and risk assessments.Pediatric research · 2025Article
- The perspective of cAMP/cGMP signaling and cyclic nucleotide phosphodiesterases in aortic aneurysm and dissection.Vascular pharmacology · 2024Review
- Marfan syndrome: insights from animal models.Frontiers in genetics · 2024Review
- 17 β-Estradiol Impedes Aortic Root Dilation and Rupture in Male Marfan Mice.International journal of molecular sciences · 2023Article
- 17 β-estradiol impedes aortic root dilation and rupture in male Marfan mice.bioRxiv : the preprint server for biology · 2023Article
- Inhibition of the Renin-Angiotensin System Fails to Suppress β-Aminopropionitrile-Induced Thoracic Aortopathy in Mice-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- Genetically engineered animal models for Marfan syndrome: challenges associated with the generation of pig models for diseases caused by haploinsufficiency.The Journal of reproduction and development · 2022Article
- Postsystolic thickening is a potential new clinical sign of injured myocardium in marfan syndrome.Scientific reports · 2021Article
- Spontaneous Right Ventricular Pseudoaneurysms and Increased Arrhythmogenicity in a Mouse Model of Marfan Syndrome.International journal of molecular sciences · 2020Article
- Pharmacologic Management of Aneurysms.Circulation research · 2019Review
- TGF-β Signaling-Related Genes and Thoracic Aortic Aneurysms and Dissections.International journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMarfan syndrome (MFS) represents a genetic disorder with variable phenotypic expression. The main cardiovascular sequelae of MFS include aortic aneurysm/dissection and cardiomyopathy. Although significant advances in the understanding of transforming growth factor beta signaling have led to promising therapeutic targets for the treatment of aortopathy, clinical studies have tempered this optimism. In particular, these studies suggest additional signaling pathways that play a significant role in disease progression. To date, studies aimed at elucidating molecular mechanisms involved in MFS-induced disease progression have been hampered by the lack of an accelerated disease model.
methodsWild-type B6.129 mice and MFS Fbn1
resultsThis accelerated murine MFS model replicates increased mortality from MFS-related maladies (20.0%, 39.3%, and 52.9% at 10, 14, and 28 days, respectively). Aortic diameters in accelerated MFS mice were significantly enlarged at 10 days after minipump implantation and correlated with a higher degree of elastin fragmentation. Accelerated MFS mice also demonstrated dilated cardiomyopathy at 14 days, even without aortic insufficiency, suggesting an intrinsic etiology.
conclusionsA novel in vivo model consisting of subcutaneously delivered angiotensin II in MFS mice reproducibly causes accelerated aortic aneurysm formation and cardiomyopathy. This model allows for better investigation of MFS sequelae by rapid experimental processes.
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