Cardiac hypertrophy: A matter of translation
Article first published online: 25 JUL 2003
Clinical and Experimental Pharmacology and Physiology
Volume 30, Issue 8, pages 517–527, August 2003
How to Cite
Hannan, R., Jenkins, A., Jenkins, A. and Brandenburger, Y. (2003), Cardiac hypertrophy: A matter of translation. Clinical and Experimental Pharmacology and Physiology, 30: 517–527. doi: 10.1046/j.1440-1681.2003.03873.x
- Issue published online: 25 JUL 2003
- Article first published online: 25 JUL 2003
- Received 7 May 2002; revision 5 November 2002; accepted 17 November 2002.
- ribosomal gene transcription;
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.