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A cell-based framework for modeling cardiac mechanics

Cardiomyocytes are the functional building blocks of the heart—yet most models developed to simulate cardiac mechanics do not represent the individual cells and their surrounding matrix. Instead, they work on a homogenized tissue level, assuming that cellular and subcellular structures and processes...

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Autores principales: Telle, Åshild, Trotter, James D., Cai, Xing, Finsberg, Henrik, Kuchta, Miroslav, Sundnes, Joakim, Wall, Samuel T.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10097778/
https://www.ncbi.nlm.nih.gov/pubmed/36602715
http://dx.doi.org/10.1007/s10237-022-01660-8
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author Telle, Åshild
Trotter, James D.
Cai, Xing
Finsberg, Henrik
Kuchta, Miroslav
Sundnes, Joakim
Wall, Samuel T.
author_facet Telle, Åshild
Trotter, James D.
Cai, Xing
Finsberg, Henrik
Kuchta, Miroslav
Sundnes, Joakim
Wall, Samuel T.
author_sort Telle, Åshild
collection PubMed
description Cardiomyocytes are the functional building blocks of the heart—yet most models developed to simulate cardiac mechanics do not represent the individual cells and their surrounding matrix. Instead, they work on a homogenized tissue level, assuming that cellular and subcellular structures and processes scale uniformly. Here we present a mathematical and numerical framework for exploring tissue-level cardiac mechanics on a microscale given an explicit three-dimensional geometrical representation of cells embedded in a matrix. We defined a mathematical model over such a geometry and parametrized our model using publicly available data from tissue stretching and shearing experiments. We then used the model to explore mechanical differences between the extracellular and the intracellular space. Through sensitivity analysis, we found the stiffness in the extracellular matrix to be most important for the intracellular stress values under contraction. Strain and stress values were observed to follow a normal-tangential pattern concentrated along the membrane, with substantial spatial variations both under contraction and stretching. We also examined how it scales to larger size simulations, considering multicellular domains. Our work extends existing continuum models, providing a new geometrical-based framework for exploring complex cell–cell and cell–matrix interactions. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10237-022-01660-8.
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spelling pubmed-100977782023-04-14 A cell-based framework for modeling cardiac mechanics Telle, Åshild Trotter, James D. Cai, Xing Finsberg, Henrik Kuchta, Miroslav Sundnes, Joakim Wall, Samuel T. Biomech Model Mechanobiol Original Paper Cardiomyocytes are the functional building blocks of the heart—yet most models developed to simulate cardiac mechanics do not represent the individual cells and their surrounding matrix. Instead, they work on a homogenized tissue level, assuming that cellular and subcellular structures and processes scale uniformly. Here we present a mathematical and numerical framework for exploring tissue-level cardiac mechanics on a microscale given an explicit three-dimensional geometrical representation of cells embedded in a matrix. We defined a mathematical model over such a geometry and parametrized our model using publicly available data from tissue stretching and shearing experiments. We then used the model to explore mechanical differences between the extracellular and the intracellular space. Through sensitivity analysis, we found the stiffness in the extracellular matrix to be most important for the intracellular stress values under contraction. Strain and stress values were observed to follow a normal-tangential pattern concentrated along the membrane, with substantial spatial variations both under contraction and stretching. We also examined how it scales to larger size simulations, considering multicellular domains. Our work extends existing continuum models, providing a new geometrical-based framework for exploring complex cell–cell and cell–matrix interactions. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10237-022-01660-8. Springer Berlin Heidelberg 2023-01-05 2023 /pmc/articles/PMC10097778/ /pubmed/36602715 http://dx.doi.org/10.1007/s10237-022-01660-8 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Original Paper
Telle, Åshild
Trotter, James D.
Cai, Xing
Finsberg, Henrik
Kuchta, Miroslav
Sundnes, Joakim
Wall, Samuel T.
A cell-based framework for modeling cardiac mechanics
title A cell-based framework for modeling cardiac mechanics
title_full A cell-based framework for modeling cardiac mechanics
title_fullStr A cell-based framework for modeling cardiac mechanics
title_full_unstemmed A cell-based framework for modeling cardiac mechanics
title_short A cell-based framework for modeling cardiac mechanics
title_sort cell-based framework for modeling cardiac mechanics
topic Original Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10097778/
https://www.ncbi.nlm.nih.gov/pubmed/36602715
http://dx.doi.org/10.1007/s10237-022-01660-8
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