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Endothelial dysfunction as a nexus for endothelial cell-cardiomyocyte miscommunication

Most studies of the heart focus on cardiomyocytes (CM) at the exclusion of other cell types such as myocardial endothelial cells (EC). Such mono-cellular approaches propagate the presumption that EC provide a mere “passive lining” or supportive role. In fact, EC contribute to a dynamic network regul...

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Detalles Bibliográficos
Autores principales: Leucker, Thorsten M., Jones, Steven P.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4144117/
https://www.ncbi.nlm.nih.gov/pubmed/25206341
http://dx.doi.org/10.3389/fphys.2014.00328
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author Leucker, Thorsten M.
Jones, Steven P.
author_facet Leucker, Thorsten M.
Jones, Steven P.
author_sort Leucker, Thorsten M.
collection PubMed
description Most studies of the heart focus on cardiomyocytes (CM) at the exclusion of other cell types such as myocardial endothelial cells (EC). Such mono-cellular approaches propagate the presumption that EC provide a mere “passive lining” or supportive role. In fact, EC contribute to a dynamic network regulating vascular tone, cardiac development, and repair. Two distinct EC types, vascular EC and epicardial EC, possess important structural and signaling properties within both the healthy and diseased myocardium. In this review, we address EC-CM interactions in mature, healthy myocardium, followed by a discussion of diseases characterized by EC dysfunction. Finally, we consider strategies to reverse EC-CM “miscommunication” to improve patients' outcomes in various cardiovascular diseases.
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spelling pubmed-41441172014-09-09 Endothelial dysfunction as a nexus for endothelial cell-cardiomyocyte miscommunication Leucker, Thorsten M. Jones, Steven P. Front Physiol Physiology Most studies of the heart focus on cardiomyocytes (CM) at the exclusion of other cell types such as myocardial endothelial cells (EC). Such mono-cellular approaches propagate the presumption that EC provide a mere “passive lining” or supportive role. In fact, EC contribute to a dynamic network regulating vascular tone, cardiac development, and repair. Two distinct EC types, vascular EC and epicardial EC, possess important structural and signaling properties within both the healthy and diseased myocardium. In this review, we address EC-CM interactions in mature, healthy myocardium, followed by a discussion of diseases characterized by EC dysfunction. Finally, we consider strategies to reverse EC-CM “miscommunication” to improve patients' outcomes in various cardiovascular diseases. Frontiers Media S.A. 2014-08-26 /pmc/articles/PMC4144117/ /pubmed/25206341 http://dx.doi.org/10.3389/fphys.2014.00328 Text en Copyright © 2014 Leucker and Jones. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Physiology
Leucker, Thorsten M.
Jones, Steven P.
Endothelial dysfunction as a nexus for endothelial cell-cardiomyocyte miscommunication
title Endothelial dysfunction as a nexus for endothelial cell-cardiomyocyte miscommunication
title_full Endothelial dysfunction as a nexus for endothelial cell-cardiomyocyte miscommunication
title_fullStr Endothelial dysfunction as a nexus for endothelial cell-cardiomyocyte miscommunication
title_full_unstemmed Endothelial dysfunction as a nexus for endothelial cell-cardiomyocyte miscommunication
title_short Endothelial dysfunction as a nexus for endothelial cell-cardiomyocyte miscommunication
title_sort endothelial dysfunction as a nexus for endothelial cell-cardiomyocyte miscommunication
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4144117/
https://www.ncbi.nlm.nih.gov/pubmed/25206341
http://dx.doi.org/10.3389/fphys.2014.00328
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