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Review
. 2011 May 1;90(2):243-50.
doi: 10.1093/cvr/cvr060. Epub 2011 Feb 25.

Taking pressure off the heart: the ins and outs of atrophic remodelling

Kedryn K Baskin  1 , Heinrich Taegtmeyer
Affiliations
Review

Taking pressure off the heart: the ins and outs of atrophic remodelling

Kedryn K Baskin et al. Cardiovasc Res. .

Abstract

Our work on atrophic remodelling of the heart has led us to appreciate the simple principles in biology: (i) the dynamic nature of intracellular protein turnover, (ii) the return to the foetal gene programme when the heart remodels, and (iii) the adaptive changes of cardiac metabolism. Although the molecular mechanisms of cardiac hypertrophy are many, much less is known regarding the molecular mechanisms of cardiac atrophy. We state the case that knowing more about mechanisms of atrophic remodelling may provide insights into cellular consequences of metabolic and haemodynamic unloading of the stressed heart. Overall we strive to find an answer to the question: 'What makes the failing heart shrink and become stronger?' We speculate that signals arising from intermediary metabolism of energy-providing substrates are likely candidates.

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Figures

Figure 1
Figure 1
Protein turnover in the heart. The balance of protein synthesis and degradation determines size and function of cardiomyocytes. Damaged, misfolded, or useless proteins are degraded to amino acids which are used for the synthesis of new, functional proteins. The amino acids phenylalanine and tyrosine (*Phe, *Tyr) are not metabolized by heart muscle and therefore used as tracers for protein synthesis and degradation in pulse-chase experiments.
Figure 2
Figure 2
Dynamic structural remodelling of cat papillary muscles in response to haemodynamic unloading and reloading. Electron micrographs of longitudinal sections under the following conditions: (A) Control; (B) 1 week of unloading; (C) 1 week of unloading, followed by 2 weeks of reloading; (D) Control, shortly after birth. The images show reversal of structural changes in heart. See text for further details. (With permission from Kent et al., JMCC 1985.)
Figure 3
Figure 3
Progressive regression of left ventricular mass after metabolic unloading by bariatric surgery. Drastic reduction in metabolic parameters (glucose, insulin, HOMA, leptin, CRP) occurs early after surgery and plateau after 9 months (metabolic unloading). Left ventricular mass continues to regress 24 months after surgery (HOMA, homeostasis model of assessment; LVM, left ventricular mass; CRP, C-reactive protein). (With permission from Algahim et al., Am J Med 2010.)
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