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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| Format: | Article |
| Language: | English |
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MDPI AG
2023-07-01
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| Series: | Cells |
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| Online Access: | https://www.mdpi.com/2073-4409/12/13/1780 |
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| author | Farhad Bazgir Julia Nau Saeideh Nakhaei-Rad Ehsan Amin Matthew J. Wolf Jeffry J. Saucerman Kristina Lorenz Mohammad Reza Ahmadian |
| author_facet | Farhad Bazgir Julia Nau Saeideh Nakhaei-Rad Ehsan Amin Matthew J. Wolf Jeffry J. Saucerman Kristina Lorenz Mohammad Reza Ahmadian |
| author_sort | Farhad Bazgir |
| collection | DOAJ |
| 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. |
| first_indexed | 2024-03-11T01:45:15Z |
| format | Article |
| id | doaj.art-7f4e41521b6542819bc73c492dd1cbe9 |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-11T01:45:15Z |
| publishDate | 2023-07-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cells |
| spelling | doaj.art-7f4e41521b6542819bc73c492dd1cbe92023-11-18T16:19:57ZengMDPI AGCells2073-44092023-07-011213178010.3390/cells12131780The Microenvironment of the Pathogenesis of Cardiac HypertrophyFarhad Bazgir0Julia Nau1Saeideh Nakhaei-Rad2Ehsan Amin3Matthew J. Wolf4Jeffry J. Saucerman5Kristina Lorenz6Mohammad Reza Ahmadian7Institute of Biochemistry and Molecular Biology II, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, 40225 Düsseldorf, GermanyInstitute of Biochemistry and Molecular Biology II, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, 40225 Düsseldorf, GermanyStem Cell Biology, and Regenerative Medicine Research Group, Institute of Biotechnology, Ferdowsi University of Mashhad, Mashhad 91779-48974, IranInstitute of Neural and Sensory Physiology, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, 40225 Düsseldorf, GermanyDepartment of Medicine and Robert M. Berne Cardiovascular Research Center, University of Virginia, Charlottesville, VA 22908, USADepartment of Biomedical Engineering, University of Virginia, Charlottesville, VA 22908, USAInstitute of Pharmacology and Toxicology, University of Würzburg, Leibniz Institute for Analytical Sciences, 97078 Würzburg, GermanyInstitute of Biochemistry and Molecular Biology II, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, 40225 Düsseldorf, GermanyPathological 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.https://www.mdpi.com/2073-4409/12/13/1780cardiac hypertrophycardiomyocytesheart failuremyocardial microenvironmentmyofibroblastspressure overload |
| spellingShingle | Farhad Bazgir Julia Nau Saeideh Nakhaei-Rad Ehsan Amin Matthew J. Wolf Jeffry J. Saucerman Kristina Lorenz Mohammad Reza Ahmadian The Microenvironment of the Pathogenesis of Cardiac Hypertrophy Cells cardiac hypertrophy cardiomyocytes heart failure myocardial microenvironment myofibroblasts pressure overload |
| 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 | cardiac hypertrophy cardiomyocytes heart failure myocardial microenvironment myofibroblasts pressure overload |
| url | https://www.mdpi.com/2073-4409/12/13/1780 |
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