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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Bibliographic Details
Published in:	Cells (Basel, Switzerland) Vol. 12; no. 13; p. 1780
Main Authors:	Bazgir, Farhad, Nau, Julia, Nakhaei-Rad, Saeideh, Amin, Ehsan, Wolf, Matthew J, Saucerman, Jeffry J, Lorenz, Kristina, Ahmadian, Mohammad Reza
Format:	Journal Article
Language:	English
Published:	Switzerland MDPI AG 01-07-2023 MDPI
Subjects:	Aged patients Analysis Aortic stenosis Arrhythmia Cardiac function cardiac hypertrophy Cardiomegaly - pathology Cardiomyocytes Cardiomyopathy Care and treatment Cell cycle Congestive heart failure Diagnosis Endothelial cells Endothelial Cells - metabolism Fibroblasts Fibrosis Growth factors Health aspects Heart attacks Heart cells Heart enlargement Heart failure Heart Failure - metabolism Humans Hypertension Hypertrophy Inflammation Mathematical models Microenvironments Musculoskeletal system myocardial microenvironment Myocardium - metabolism Myocytes, Cardiac - metabolism myofibroblasts Pathogenesis Peptides Physiological aspects Physiology Pregnancy pressure overload Proteins Review Risk factors Smooth muscle Stress (Physiology) Vasoactive agents Germany cardiomyocytes heart failure myocardial microenvironment cardiac hypertrophy vasoactive hormones myofibroblasts pressure overload scar formation
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Summary:	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.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 These authors contributed equally to this work.
ISSN:	2073-4409 2073-4409
DOI:	10.3390/cells12131780