ArticlePLoS computational biology2020
Numerical knockouts-In silico assessment of factors predisposing to thoracic aortic aneurysms.
Article in PLoS computational biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- The aorta in Marfan syndrome: from molecular mechanisms to mechanobiological dysfunction.Cardiovascular research · 2026Review
- Hypertension drives thoracic aortic aneurysm and dissection in male, but not female, Marfan mice.Journal of the mechanical behavior of biomedical materials · 2026Article
- Impact of Dynamic Axial Stretching on the Arterial Pulse Wave Velocity: Physical Foundation and Clinical Implications.Annals of biomedical engineering · 2026Article
- Mechanisms driving thoracic aortic aneurysm instability.Biomechanics and modeling in mechanobiology · 2026Article
- Systematic Disruption of Zebrafish Fibrillin Genes Identifies a Translational Zebrafish Model for Marfan Syndrome.JACC. Basic to translational science · 2026Article
- Physics-Based Growth and Remodeling Modeling for Virtual Abdominal Aortic Aneurysm Evolution and Growth Prediction.medRxiv : the preprint server for health sciences · 2026Article
- Mechanisms Driving Thoracic Aortic Aneurysm Stability.bioRxiv : the preprint server for biology · 2025Article
- Importance of localized dilatation and distensibility in identifying determinants of thoracic aortic aneurysm with neural operators.PLoS computational biology · 2025Article
- Changes in Gene Expression Patterns in Young and Senescent Fibroblasts in Glycated Three-Dimensional Collagen Matrices.International journal of molecular sciences · 2025Article
- Short-term disruption of TGF-β signaling in adult mice renders the aorta vulnerable to hypertension-induced dissection.JCI insight · 2025Article
- FSGe: A fast and strongly-coupled 3D fluid-solid-growth interaction method.Computer methods in applied mechanics and engineering · 2024Article
- A computational growth and remodeling framework for adaptive and maladaptive pulmonary arterial hemodynamics.Biomechanics and modeling in mechanobiology · 2023Article
- Effects of Age, Sex, and Extracellular Matrix Integrity on Aortic Dilatation and Rupture in a Mouse Model of Marfan Syndrome.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Computational modelling distinguishes diverse contributors to aneurysmal progression in the Marfan aorta.Proceedings. Mathematical, physical, and engineering sciences · 2023Article
- A Computational Growth and Remodeling Framework for Adaptive and Maladaptive Pulmonary Arterial Hemodynamics.bioRxiv : the preprint server for biology · 2023Article
- Computational analysis of the role of mechanosensitive Notch signaling in arterial adaptation to hypertension.Journal of the mechanical behavior of biomedical materials · 2022Article
- Neural operator learning of heterogeneous mechanobiological insults contributing to aortic aneurysms.Journal of the Royal Society, Interface · 2022Article
- Evolving Mural Defects, Dilatation, and Biomechanical Dysfunction in Angiotensin II-Induced Thoracic Aortopathies.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- In vivo development of tissue engineered vascular grafts: a fluid-solid-growth model.Biomechanics and modeling in mechanobiology · 2022Article
- Bayesian calibration of a computational model of tissue expansion based on a porcine animal model.Acta biomaterialia · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Myriad risk factors-including uncontrolled hypertension, aging, and diverse genetic mutations-contribute to the development and enlargement of thoracic aortic aneurysms. Detailed analyses of clinical data and longitudinal studies of murine models continue to provide insight into the natural history of these potentially lethal conditions. Yet, because of the co-existence of multiple risk factors in most cases, it has been difficult to isolate individual effects of the many different factors or to understand how they act in combination. In this paper, we use a data-informed computational model of the initiation and progression of thoracic aortic aneurysms to contrast key predisposing risk factors both in isolation and in combination; these factors include localized losses of elastic fiber integrity, aberrant collagen remodeling, reduced smooth muscle contractility, and dysfunctional mechanosensing or mechanoregulation of extracellular matrix along with superimposed hypertension and aortic aging. In most cases, mild-to-severe localized losses in cellular function or matrix integrity give rise to varying degrees of local dilatations of the thoracic aorta, with enlargement typically exacerbated in cases wherein predisposing risk factors co-exist. The simulations suggest, for the first time, that effects of compromised smooth muscle contractility are more important in terms of dysfunctional mechanosensing and mechanoregulation of matrix than in vessel-level control of diameter and, furthermore, that dysfunctional mechanobiological control can yield lesions comparable to those in cases of compromised elastic fiber integrity. Particularly concerning, therefore, is that loss of constituents such as fibrillin-1, as in Marfan syndrome, can compromise both elastic fiber integrity and mechanosensing.
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Registered trials
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