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The endocrinological component and signaling pathways associated to cardiac hypertrophy

Although myocardial growth corresponds to an adaptive response to maintain cardiac contractile function, the cardiac hypertrophy is a condition that occurs in many cardiovascular diseases and typically precedes the onset of heart failure. Different endocrine factors such as thyroid hormones, insulin...

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Published in:Molecular and cellular endocrinology 2020-12, Vol.518, p.110972-110972, Article 110972
Main Authors: Takano, Ana Paula Cremasco, Senger, Nathalia, Barreto-Chaves, Maria Luiza M.
Format: Article
Language:English
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Summary:Although myocardial growth corresponds to an adaptive response to maintain cardiac contractile function, the cardiac hypertrophy is a condition that occurs in many cardiovascular diseases and typically precedes the onset of heart failure. Different endocrine factors such as thyroid hormones, insulin, insulin-like growth factor 1 (IGF-1), angiotensin II (Ang II), endothelin (ET-1), catecholamines, estrogen, among others represent important stimuli to cardiomyocyte hypertrophy. Thus, numerous endocrine disorders manifested as changes in the local environment or multiple organ systems are especially important in the context of progression from cardiac hypertrophy to heart failure. Based on that information, this review summarizes experimental findings regarding the influence of such hormones upon signalling pathways associated with cardiac hypertrophy. Understanding mechanisms through which hormones differentially regulate cardiac hypertrophy could open ways to obtain therapeutic approaches that contribute to prevent or delay the onset of heart failure related to endocrine diseases. •Endocrine stimuli can lead to increase of cardiomyocyte volume inducing to a cardiac hypertrophic phenotype.•The development of cardiac hypertrophy by endocrine factors occurs by activation of distinct cellular signaling or multiple interconnected signaling pathways.•Here, some endocrine factors and their signaling pathways responsible for physiological or pathological cardiac hypertrophy are addressed.
ISSN:0303-7207
1872-8057
DOI:10.1016/j.mce.2020.110972