ArticleJournal of the American Heart Association2015
Development of Aortic Valve Disease in Familial Hypercholesterolemic Swine: Implications for Elucidating Disease Etiology.
Article in Journal of the American Heart Association, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- Aortic valve disease: Novel animal models for advancing our understanding of the underlying mechanisms.Animal models and experimental medicine · 2026Review
- Trimethylamine-N-oxide promotes fibrotic activation of quiescent valvular interstitial cells via endoplasmic reticulum stress.Scientific reports · 2025Article
- Deciphering the Enigma of Calcific Aortic Valve Disease: The Pivotal Role of Animal Models in Unraveling Pathogenesis and Advancing Therapeutic Strategies.Biomedicines · 2025Review
- Insights into preclinical models of calcific aortic valve disease and their translational potential.Frontiers in cardiovascular medicine · 2025Review
- Oxidative low-density lipoprotein and shear induced calcification within a calcific aortic valve disease-on-a-chip platform.Frontiers in cardiovascular medicine · 2025Article
- Pulse wave and vector flow Imaging for atherosclerotic disease progression in hypercholesterolemic swine.Scientific reports · 2023Article
- Models and Techniques to Study Aortic Valve CalcificationFrontiers in pharmacology · 2022Review
- Glycosaminoglycans affect endothelial to mesenchymal transformation, proliferation, and calcification in a 3D model of aortic valve disease.Frontiers in cardiovascular medicine · 2022Article
- Engineering the aortic valve extracellular matrix through stages of development, aging, and disease.Journal of molecular and cellular cardiology · 2021Review
- Effects of Altering Mitochondrial Antioxidant Capacity on Molecular and Phenotypic Drivers of Fibrocalcific Aortic Valve Stenosis.Frontiers in cardiovascular medicine · 2021Article
- Angiogenic Secretion Profile of Valvular Interstitial Cells Varies With Cellular Sex and Phenotype.Frontiers in cardiovascular medicine · 2021Article
- Metabolomic Signature of Human Aortic Valve Stenosis.JACC. Basic to translational science · 2020Article
- Disease-inspired tissue engineering: Investigation of cardiovascular pathologies.ACS biomaterials science & engineering · 2020Review
- Creation of disease-inspired biomaterial environments to mimic pathological events in early calcific aortic valve disease.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Advances in Pathophysiology of Calcific Aortic Valve Disease Propose Novel Molecular Therapeutic Targets.Frontiers in cardiovascular medicine · 2018Article
- Effect of Caloric Restriction on Metabolic Dysfunction of Young Rapacz Familial Hypercholesterolemic Swine (Comparative medicine · 2017Article
- Dysregulation of hyaluronan homeostasis during aortic valve disease.Matrix biology : journal of the International Society for Matrix Biology · 2017Article
- Robust Generation of Quiescent Porcine Valvular Interstitial Cell Cultures.Journal of the American Heart Association · 2017Article
- Epigenome alterations in aortic valve stenosis and its related left ventricular hypertrophy.Clinical epigenetics · 2017Review
- Development of Aortic Valve Disease in Familial Hypercholesterolemic Swine: Implications for Elucidating Disease Etiology.Journal of the American Heart Association · 2015Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundFamilial hypercholesterolemia (FH) is a prevalent hereditary disease associated with increased atherosclerosis and calcific aortic valve disease (CAVD). However, in both FH and non-FH individuals, the role of hypercholesterolemia in the development of CAVD is poorly understood. This study used Rapacz FH (RFH) swine, an established model of human FH, to investigate the role of hypercholesterolemia alone in the initiation and progression of CAVD. The valves of RFH swine have not previously been examined. METHODS AND
resultsAortic valve leaflets were isolated from wild-type (0.25- and 1-year-old) and RFH (0.25-, 1-, 2-, and 3-year-old) swine. Adult RFH animals exhibited numerous hallmarks of early CAVD. Significant leaflet thickening was found in adult RFH swine, accompanied by extensive extracellular matrix remodeling, including proteoglycan enrichment, collagen disorganization, and elastin fragmentation. Increased lipid oxidation and infiltration of macrophages were also evident in adult RFH swine. Intracardiac echocardiography revealed mild aortic valve sclerosis in some of the adult RFH animals, but unimpaired valve function. Microarray analysis of valves from adult versus juvenile RFH animals revealed significant upregulation of inflammation-related genes, as well as several commonalities with atherosclerosis and overlap with human CAVD.
conclusionsAdult RFH swine exhibited several hallmarks of early human CAVD, suggesting potential for these animals to help elucidate CAVD etiology in both FH and non-FH individuals. The development of advanced atherosclerotic lesions, but only early-stage CAVD, in RFH swine supports the hypothesis of an initial shared disease process, with additional stimulation necessary for further progression of CAVD.
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What Socratic holds
Registered trials
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.