A mathematical model of mechanotransduction

This article reviews the mechanical bidomain model, a mathematical description of how the extracellular matrix and intracellular cytoskeleton of cardiac tissue are coupled by integrin membrane proteins. The fundamental hypothesis is that the difference between the intracellular and extrac...

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Main Author: Bradley J. Roth
Format: Article
Language:English
Published: Academia.edu Journals 2023-03-01
Series:Academia Biology
Online Access:https://www.academia.edu/98963202/A_mathematical_model_of_mechanotransduction
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author Bradley J. Roth
author_facet Bradley J. Roth
author_sort Bradley J. Roth
collection DOAJ
description This article reviews the mechanical bidomain model, a mathematical description of how the extracellular matrix and intracellular cytoskeleton of cardiac tissue are coupled by integrin membrane proteins. The fundamental hypothesis is that the difference between the intracellular and extracellular displacements drives mechanotransduction. A one-dimensional example illustrates the model, which is then extended to two or three dimensions. In a few cases, the bidomain equations can be solved analytically, demonstrating how tissue motion can be divided into two parts: monodomain displacements that are the same in both spaces and therefore do not contribute to mechanotransduction, and bidomain displacements that cause mechanotransduction. The model contains a length constant that depends on the intracellular and extracellular shear moduli and the integrin spring constant. Bidomain effects often occur within a few length constants of the tissue edge. Unequal anisotropy ratios in the intra- and extracellular spaces can modulate mechanotransduction. Insight into model predictions is supplied by simple analytical examples, such as the shearing of a slab of cardiac tissue or the contraction of a tissue sheet. Computational methods for solving the model equations are described, and precursors to the model are reviewed. Potential applications are discussed, such as predicting growth and remodeling in the diseased heart, analyzing stretch-induced arrhythmias, modeling shear forces in a vessel caused by blood flow, examining the role of mechanical forces in engineered sheets of tissue, studying differentiation in colonies of stem cells, and characterizing the response to localized forces applied to nanoparticles.
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spelling doaj-art-d05d6bbb336d4ecdb018aecd7d654ab42025-02-10T23:12:27ZengAcademia.edu JournalsAcademia Biology2837-40102023-03-011110.20935/AcadBiol6081A mathematical model of mechanotransductionBradley J. Roth0Department of Physics, Oakland University, Rochester, MI, USA. This article reviews the mechanical bidomain model, a mathematical description of how the extracellular matrix and intracellular cytoskeleton of cardiac tissue are coupled by integrin membrane proteins. The fundamental hypothesis is that the difference between the intracellular and extracellular displacements drives mechanotransduction. A one-dimensional example illustrates the model, which is then extended to two or three dimensions. In a few cases, the bidomain equations can be solved analytically, demonstrating how tissue motion can be divided into two parts: monodomain displacements that are the same in both spaces and therefore do not contribute to mechanotransduction, and bidomain displacements that cause mechanotransduction. The model contains a length constant that depends on the intracellular and extracellular shear moduli and the integrin spring constant. Bidomain effects often occur within a few length constants of the tissue edge. Unequal anisotropy ratios in the intra- and extracellular spaces can modulate mechanotransduction. Insight into model predictions is supplied by simple analytical examples, such as the shearing of a slab of cardiac tissue or the contraction of a tissue sheet. Computational methods for solving the model equations are described, and precursors to the model are reviewed. Potential applications are discussed, such as predicting growth and remodeling in the diseased heart, analyzing stretch-induced arrhythmias, modeling shear forces in a vessel caused by blood flow, examining the role of mechanical forces in engineered sheets of tissue, studying differentiation in colonies of stem cells, and characterizing the response to localized forces applied to nanoparticles.https://www.academia.edu/98963202/A_mathematical_model_of_mechanotransduction
spellingShingle Bradley J. Roth
A mathematical model of mechanotransduction
Academia Biology
title A mathematical model of mechanotransduction
title_full A mathematical model of mechanotransduction
title_fullStr A mathematical model of mechanotransduction
title_full_unstemmed A mathematical model of mechanotransduction
title_short A mathematical model of mechanotransduction
title_sort mathematical model of mechanotransduction
url https://www.academia.edu/98963202/A_mathematical_model_of_mechanotransduction
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