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Cardiac hypertrophy: a matter of translation
R D Hannan1, A Jenkins, A K Jenkins
1Gene Transcription Laboratory, Baker Medical Research Institute, Melbourne, Victoria, Australia.
Insights
Left ventricular hypertrophy (LVH) involves cardiac muscle cells (cardiomyocytes) increasing in size, not number. This adaptive response to heart strain is driven by protein synthesis changes within these cells.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Cellular Physiology
Background:
- Left ventricular hypertrophy (LVH) is a cardiac adaptation to sustained hypertension and hormonal imbalances.
- LVH involves molecular and biochemical changes in cardiomyocytes, fibroblasts, conductive tissue, and coronary vasculature.
- Cellular hypertrophy, an increase in cardiomyocyte size without proliferation, drives heart chamber enlargement in LVH.
Purpose of the Study:
- To review the mechanisms of protein synthesis regulation in cardiomyocytes during hypertrophy.
- To examine the roles of translational capacity and translational efficiency in cardiomyocyte growth.
- To elucidate the contribution of these protein synthesis mechanisms to the development of LVH.
Main Methods:
- Review of existing literature on cardiomyocyte hypertrophy and protein synthesis.
- Analysis of molecular and biochemical responses in cardiac cells.
- Examination of translational control mechanisms (capacity vs. efficiency).
Main Results:
- Cardiomyocyte hypertrophy increases cell size, not number, contributing to LVH.
- Accelerated global protein synthesis drives protein accumulation in hypertrophic cardiomyocytes.
- Increased protein synthesis results from enhanced translational efficiency and/or capacity.
Conclusions:
- Both translational capacity and efficiency are crucial for cardiomyocyte response to increased protein synthesis demands.
- Understanding these mechanisms is key to comprehending LVH development.
- Further research into translational control could reveal therapeutic targets for LVH.
Abstract:
1. Left ventricular hypertrophy (LVH) of the heart is an adaptive response to sustained increases in blood pressure and hormone imbalances. Left ventricular hypertrophy is associated with programmed responses at the molecular and biochemical level in different subsets of cardiac cells, including the cardiac muscle cells (cardiomyocytes), fibroblasts, conductive tissue and coronary vasculature. 2. Regardless of the initiating cause, the actual increase in chamber enlargement is, in each case, due to an increase in size of a pre-existing cardiomyocyte population, with little or no change in their number; a process referred to as cellular hypertrophy. 3. An accelerated rate of global protein synthesis is the primary mechanism by which protein accumulation increases during cardiomyocyte hypertrophy. In turn, increased rates of synthesis are a result of increased translational rates of existing ribosomes (translational efficiency) and/or synthesis and recruitment of additional ribosomes (translational capacity). 4. The present review examines the relative importance of translational capacity and translational efficiency in the response of myocytes to acute and chronic demands for increased protein synthesis and the role of these mechanisms in the development of LVH.
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