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Journal Article
Molecular basis of physiological heart growth: fundamental concepts and new players
2013
Overview
Key Points
Physiological hypertrophy is an adaptive form of cardiac hypertrophy that does not lead to heart disease in healthy individuals.
This cardiac growth maintains or augments cardiac function and increases angiogenesis and metabolism. Physiological hypertrophy does not promote fibrotic remodelling or cardiomyocyte death.
Physiological hypertrophy is initiated by specific hormones (triiodothyronine, insulin, insulin-like growth factor 1 and vascular endothelial growth factor) or stretch (loading), which activate a restricted number of intracellular signalling pathways (PI3K, AKT, mTOR and ERK1/2).
Metabolic reprogramming governed by AMP-activated protein kinase (AMPK) is essential for adaptive cardiac hypertrophy.
Exercise induced hypertrophy causes a downregulation of CCAAT/enhancer binding protein-β and the transcription of an exercise-specific gene set.
Intermittent PI3K, AKT, ERK1/2 or AMPK activation promotes the activation of a physiological hypertrophic programme to maintain or augment function, thus antagonizing pathological conditions.
The heart undergoes physiological hypertrophy in response to developmental signals and increased workload. The structural and molecular characteristics of physiological cardiac hypertrophy are now being elucidated, as are the endocrine effectors and associated signalling pathways that regulate it.
The heart hypertrophies in response to developmental signals as well as increased workload. Although adult-onset hypertrophy can ultimately lead to disease, cardiac hypertrophy is not necessarily maladaptive and can even be beneficial. Progress has been made in our understanding of the structural and molecular characteristics of physiological cardiac hypertrophy, as well as of the endocrine effectors and associated signalling pathways that regulate it. Physiological hypertrophy is initiated by finite signals, which include growth hormones (such as thyroid hormone, insulin, insulin-like growth factor 1 and vascular endothelial growth factor) and mechanical forces that converge on a limited number of intracellular signalling pathways (such as PI3K, AKT, AMP-activated protein kinase and mTOR) to affect gene transcription, protein translation and metabolism. Harnessing adaptive signalling mediators to reinvigorate the diseased heart could have important medical ramifications.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
