ArticleInternational journal of engineering science2019
Computational Modeling Predicts Immuno-Mechanical Mechanisms of Maladaptive Aortic Remodeling in Hypertension.
Article in International journal of engineering science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Predicted Effects of Patient Variability and Notch Signaling on In Situ Vascular Tissue Engineering.Annals of biomedical engineering · 2026Article
- Multi-Scale Multi-Cell Computational Model of Inflammation-Mediated Aortic Remodeling in Hypertension.Annals of biomedical engineering · 2025Article
- Computational model of coarctation of the aorta in rabbits suggests persistent ascending aortic remodeling post-correction.Biomechanics and modeling in mechanobiology · 2025Article
- Multiscale homogenized constrained mixture model of the bio-chemo-mechanics of soft tissue growth and remodeling.Biomechanics and modeling in mechanobiology · 2024Article
- Beyond CFD: Emerging methodologies for predictive simulation in cardiovascular health and disease.Biophysics reviews · 2023Review
- Irregular anatomical features can alter hemodynamics in Takayasu arteritis.JVS-vascular science · 2023Article
- Computational analysis of the role of mechanosensitive Notch signaling in arterial adaptation to hypertension.Journal of the mechanical behavior of biomedical materials · 2022Article
- Tissue engineered vascular grafts transform into autologous neovessels capable of native function and growth.Communications medicine · 2022Article
- Constrained Mixture Models of Soft Tissue Growth and Remodeling - Twenty Years After.Journal Of Elasticity · 2021Article
- Vascular Mechanobiology: Homeostasis, Adaptation, and Disease.Annual review of biomedical engineering · 2021Review
- Mechanisms of Vascular Remodeling in Hypertension.American journal of hypertension · 2021Review
- Computational models of cardiac hypertrophy.Progress in biophysics and molecular biology · 2021Review
- Complementary roles of mechanotransduction and inflammation in vascular homeostasis.Proceedings. Mathematical, physical, and engineering sciences · 2021Article
- Plasma Metabolomics Analysis Identifies Abnormal Energy, Lipid, and Amino Acid Metabolism in Abdominal Aortic Aneurysms.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Numerical knockouts-In silico assessment of factors predisposing to thoracic aortic aneurysms.PLoS computational biology · 2020Article
- Vascular adaptation in the presence of external support - A modeling study.Journal of the mechanical behavior of biomedical materials · 2020Article
- Cell signaling model for arterial mechanobiology.PLoS computational biology · 2020Article
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Authors and funding
3 authors at 2 institutions in 1 country.
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Abstract
Uncontrolled hypertension is a major risk factor for myriad cardiovascular diseases. Among its many effects, hypertension increases central artery stiffness which in turn is both an initiator and indicator of disease. Despite extensive clinical, animal, and basic science studies, the biochemomechanical mechanisms by which hypertension drives aortic stiffening remain unclear. In this paper, we show that a new computational model of aortic growth and remodeling can capture differential effects of induced hypertension on the thoracic and abdominal aorta in a common mouse model of disease. Because the simulations treat the aortic wall as a constrained mixture of different constituents having different material properties and rates of turnover, one can gain increased insight into underlying constituent-level mechanisms of aortic remodeling. Model results suggest that the aorta can mechano-adapt locally to blood pressure elevation in the absence of marked inflammation, but large increases in inflammation drive a persistent maladaptive phenotype characterized primarily by adventitial fibrosis. Moreover, this fibrosis appears to occur via a marked increase in the rate of deposition of collagen having different material properties in the absence of a compensatory increase in the rate of matrix degradation. Controlling inflammation thus appears to be key to reducing fibrosis, but therapeutic strategies should not compromise the proteolytic activity of the wall that is essential to mechanical homeostasis.
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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.