IMR Press / FBL / Volume 13 / Issue 1 / DOI: 10.2741/2681

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Article
Physiological myocardial hypertrophy: how and why?
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1 Department of Medicine, Division of Cardiology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA
2 Science and Technology Pole, IRCCS MultiMedica Hospital, Via Fantoli 16/15, 20100, Milan, Italy
3 Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway
4 Department of Cardiology, St. Olavs Hospital, Trondheim, Norway
Front. Biosci. (Landmark Ed) 2008, 13(1), 312–324; https://doi.org/10.2741/2681
Published: 1 January 2008
Abstract

Cardiac hypertrophy is defined by augmentation of ventricular mass as a result of increased cardiomyocyte size, and is the adaptive response of the heart to enhanced hemodynamic loads due to either physiological stimuli (post-natal developmental growth, training, and pregnancy) or pathological states (such as hypertension, valvular insufficiency, etc). The mechanisms leading to hypertrophy during pathological and physiological states are distinct but, in general, evidence indicates that hypertrophy results from the interaction of mechanical forces and neurohormonal factors. Hemodynamic overload creates a mechanical burden on the heart and results in stretch of the myocyte and induction of gene expression of cardiac growth factors. Insulin-like growth factor 1 (IGF1) has recently been shown to be the most important cardiac growth factor involved in physiological hypertrophy. In this review, IGF1 and the pathways it triggers will be discussed.

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