ArticleClinical research in cardiology : official journal of the German Cardiac Society2019
Graded murine wire-induced aortic valve stenosis model mimics human functional and morphological disease phenotype.
Article in Clinical research in cardiology : official journal of the German Cardiac Society, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 38 citations in OpenAlex.
- Aortic valve disease: Novel animal models for advancing our understanding of the underlying mechanisms.Animal models and experimental medicine · 2026Review
- Glycoursodeoxycholic acid 3 sulfate sodium links hemodynamics and bile acid metabolism in aortic stenosis.Journal of advanced research · 2026Article
- Considerations in the Use of Mouse Models of Vascular and Valvular Calcification.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Calcific aortic valve disease augments vesicular microRNA-145-5p to regulate the calcification of valvular interstitial cells via cellular crosstalk.Basic research in cardiology · 2025Article
- Sex differences in a murine model of infective endocarditis.Basic research in cardiology · 2025Article
- Deciphering the Enigma of Calcific Aortic Valve Disease: The Pivotal Role of Animal Models in Unraveling Pathogenesis and Advancing Therapeutic Strategies.Biomedicines · 2025Review
- Aortic valve stenosis and osteoporosis: insights from a mouse model.BMC cardiovascular disorders · 2025Article
- Article
- Novel Humanized Aortic Valve Calcification Model.Circulation research · 2025Article
- A murine model of aortic regurgitation generated by trans-apical wire destruction of the aortic valve.Animal models and experimental medicine · 2025Article
- Nutrient restriction protects against valve interstitial cell calcification by upregulating ubiquitin mediated proteolysis.Frontiers in cardiovascular medicine · 2025Article
- A novel approach to studying infective endocarditis: Ultrasound-guided wire injury and bacterial challenge in mice.PloS one · 2025Article
- A novel mouse model of calcific aortic valve stenosis.Animal models and experimental medicine · 2024Article
- Toll-like receptor-3 contributes to the development of aortic valve stenosis.Basic research in cardiology · 2023Article
- Platelet membrane-coated alterbrassicene A nanoparticle inhibits calcification of the aortic valve by suppressing phosphorylation P65 NF-κB.Theranostics · 2023Article
- Wall shear stress and its role in atherosclerosis.Frontiers in cardiovascular medicine · 2023Review
- PTP1B Inhibition Improves Mitochondrial Dynamics to Alleviate Calcific Aortic Valve Disease Via Regulating OPA1 Homeostasis.JACC. Basic to translational science · 2022Article
- Multiparametric MRI identifies subtle adaptations for demarcation of disease transition in murine aortic valve stenosis.Basic research in cardiology · 2022Article
- Models and Techniques to Study Aortic Valve CalcificationFrontiers in pharmacology · 2022Review
- S2 Heart Sound Detects Aortic Valve Calcification Independent of Hemodynamic Changes in Mice.Frontiers in cardiovascular medicine · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aortic valve stenosis (AS) is the most common valve disease requiring therapeutic intervention. Even though the incidence of AS has been continuously rising and AS is associated with significant morbidity and mortality, to date, no medical treatments have been identified that can modify disease progression. This unmet medical need is likely attributed to an incomplete understanding of the molecular mechanism driving disease development. To investigate the pathophysiology leading to AS, reliable and reproducible animal models that mimic human pathophysiology are needed. We have tested and expanded the protocols of a wire-injury induced AS mouse model. For this model, coronary wires were used to apply shear stress to the aortic valve cusps with increasing intensity. These protocols allowed distinction of mild, moderate and severe wire-injury. Upon moderate or severe injury, AS developed with a significant increase in aortic valve peak blood flow velocity. While moderate injury promoted solitary AS, severe-injury induced mixed aortic valve disease with concomitant mild to moderate aortic regurgitation. The changes in aortic valve function were reflected by dilation and hypertrophy of the left ventricle, as well as a decreased left ventricular ejection fraction. Histological analysis revealed the classic hallmarks of human disease with aortic valve thickening, increased macrophage infiltration, fibrosis and calcification. This new mouse model of AS promotes functional and morphological changes similar to moderate and severe human AS. It can be used to investigate the pathomechanisms contributing to AS development and to test novel therapeutic strategies.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.