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The Microenvironment of the Pathogenesis of Cardiac Hypertrophy

Pathological cardiac hypertrophy is a key risk factor for the development of heart failure and predisposes individuals to cardiac arrhythmia and sudden death. While physiological cardiac hypertrophy is adaptive, hypertrophy resulting from conditions comprising hypertension, aortic stenosis, or genet...

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Autores principales: Bazgir, Farhad, Nau, Julia, Nakhaei-Rad, Saeideh, Amin, Ehsan, Wolf, Matthew J., Saucerman, Jeffry J., Lorenz, Kristina, Ahmadian, Mohammad Reza
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10341218/
https://www.ncbi.nlm.nih.gov/pubmed/37443814
http://dx.doi.org/10.3390/cells12131780
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author Bazgir, Farhad
Nau, Julia
Nakhaei-Rad, Saeideh
Amin, Ehsan
Wolf, Matthew J.
Saucerman, Jeffry J.
Lorenz, Kristina
Ahmadian, Mohammad Reza
author_facet Bazgir, Farhad
Nau, Julia
Nakhaei-Rad, Saeideh
Amin, Ehsan
Wolf, Matthew J.
Saucerman, Jeffry J.
Lorenz, Kristina
Ahmadian, Mohammad Reza
author_sort Bazgir, Farhad
collection PubMed
description Pathological cardiac hypertrophy is a key risk factor for the development of heart failure and predisposes individuals to cardiac arrhythmia and sudden death. While physiological cardiac hypertrophy is adaptive, hypertrophy resulting from conditions comprising hypertension, aortic stenosis, or genetic mutations, such as hypertrophic cardiomyopathy, is maladaptive. Here, we highlight the essential role and reciprocal interactions involving both cardiomyocytes and non-myocardial cells in response to pathological conditions. Prolonged cardiovascular stress causes cardiomyocytes and non-myocardial cells to enter an activated state releasing numerous pro-hypertrophic, pro-fibrotic, and pro-inflammatory mediators such as vasoactive hormones, growth factors, and cytokines, i.e., commencing signaling events that collectively cause cardiac hypertrophy. Fibrotic remodeling is mediated by cardiac fibroblasts as the central players, but also endothelial cells and resident and infiltrating immune cells enhance these processes. Many of these hypertrophic mediators are now being integrated into computational models that provide system-level insights and will help to translate our knowledge into new pharmacological targets. This perspective article summarizes the last decades’ advances in cardiac hypertrophy research and discusses the herein-involved complex myocardial microenvironment and signaling components.
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spelling pubmed-103412182023-07-14 The Microenvironment of the Pathogenesis of Cardiac Hypertrophy Bazgir, Farhad Nau, Julia Nakhaei-Rad, Saeideh Amin, Ehsan Wolf, Matthew J. Saucerman, Jeffry J. Lorenz, Kristina Ahmadian, Mohammad Reza Cells Review Pathological cardiac hypertrophy is a key risk factor for the development of heart failure and predisposes individuals to cardiac arrhythmia and sudden death. While physiological cardiac hypertrophy is adaptive, hypertrophy resulting from conditions comprising hypertension, aortic stenosis, or genetic mutations, such as hypertrophic cardiomyopathy, is maladaptive. Here, we highlight the essential role and reciprocal interactions involving both cardiomyocytes and non-myocardial cells in response to pathological conditions. Prolonged cardiovascular stress causes cardiomyocytes and non-myocardial cells to enter an activated state releasing numerous pro-hypertrophic, pro-fibrotic, and pro-inflammatory mediators such as vasoactive hormones, growth factors, and cytokines, i.e., commencing signaling events that collectively cause cardiac hypertrophy. Fibrotic remodeling is mediated by cardiac fibroblasts as the central players, but also endothelial cells and resident and infiltrating immune cells enhance these processes. Many of these hypertrophic mediators are now being integrated into computational models that provide system-level insights and will help to translate our knowledge into new pharmacological targets. This perspective article summarizes the last decades’ advances in cardiac hypertrophy research and discusses the herein-involved complex myocardial microenvironment and signaling components. MDPI 2023-07-04 /pmc/articles/PMC10341218/ /pubmed/37443814 http://dx.doi.org/10.3390/cells12131780 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Bazgir, Farhad
Nau, Julia
Nakhaei-Rad, Saeideh
Amin, Ehsan
Wolf, Matthew J.
Saucerman, Jeffry J.
Lorenz, Kristina
Ahmadian, Mohammad Reza
The Microenvironment of the Pathogenesis of Cardiac Hypertrophy
title The Microenvironment of the Pathogenesis of Cardiac Hypertrophy
title_full The Microenvironment of the Pathogenesis of Cardiac Hypertrophy
title_fullStr The Microenvironment of the Pathogenesis of Cardiac Hypertrophy
title_full_unstemmed The Microenvironment of the Pathogenesis of Cardiac Hypertrophy
title_short The Microenvironment of the Pathogenesis of Cardiac Hypertrophy
title_sort microenvironment of the pathogenesis of cardiac hypertrophy
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10341218/
https://www.ncbi.nlm.nih.gov/pubmed/37443814
http://dx.doi.org/10.3390/cells12131780
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