ArticleBiomechanics and modeling in mechanobiology2023
A computational growth and remodeling framework for adaptive and maladaptive pulmonary arterial hemodynamics.
Article in Biomechanics and modeling in mechanobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 12 citations in OpenAlex.
- A microstructurally motivated framework to study autoregulation in the coronary circulation.The Journal of physiology · 2026Article
- Postnatal pulmonary artery development from transcript to tissue.Journal of the Royal Society, Interface · 2026Article
- Baseline state for pulmonary vasculature with pulmonary arterial hypertension: effect of geometric remodeling and metabolic shift.Biomechanics and modeling in mechanobiology · 2026Article
- Vascular Remodelling in COPD: An In Silico Tool to Represent Pulmonary Haemodynamics in Obstructive Lung Disease.Annals of biomedical engineering · 2026Article
- A second-hit conceptual framework for pulmonary arterial hypertension in adult congenital heart disease: genetics, hemodynamics, and treat-and-repair.Frontiers in cardiovascular medicine · 2026Review
- A Brief Overview of Biomechanics and Mechanobiology of the Pulmonary Circulation.Advances in experimental medicine and biology · 2026Review
- A Microstructurally-Motivated Framework to Study Autoregulation in the Coronary Circulation.bioRxiv : the preprint server for biology · 2025Article
- High Shear Stress Reduces ERG Causing Endothelial-Mesenchymal Transition and Pulmonary Arterial Hypertension.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Biomechanics of soft biological tissues and organs, mechanobiology, homeostasis and modelling.Journal of the Royal Society, Interface · 2025Review
- FSGe: A fast and strongly-coupled 3D fluid-solid-growth interaction method.Computer methods in applied mechanics and engineering · 2024Article
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Authors and funding
5 authors at 2 institutions in 1 country.
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Abstract
Hemodynamic loading is known to contribute to the development and progression of pulmonary arterial hypertension (PAH). This loading drives changes in mechanobiological stimuli that affect cellular phenotypes and lead to pulmonary vascular remodeling. Computational models have been used to simulate mechanobiological metrics of interest, such as wall shear stress, at single time points for PAH patients. However, there is a need for new approaches that simulate disease evolution to allow for prediction of long-term outcomes. In this work, we develop a framework that models the pulmonary arterial tree through adaptive and maladaptive responses to mechanical and biological perturbations. We coupled a constrained mixture theory-based growth and remodeling framework for the vessel wall with a morphometric tree representation of the pulmonary arterial vasculature. We show that non-uniform mechanical behavior is important to establish the homeostatic state of the pulmonary arterial tree, and that hemodynamic feedback is essential for simulating disease time courses. We also employed a series of maladaptive constitutive models, such as smooth muscle hyperproliferation and stiffening, to identify critical contributors to development of PAH phenotypes. Together, these simulations demonstrate an important step toward predicting changes in metrics of clinical interest for PAH patients and simulating potential treatment approaches.
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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 Socratic graph.