The heart is one of the highest ATP consuming organs in mammalian organisms. Its metabolic function has evolved a remarkable degree of efficiency to meet high demand and plasticity in response to varying changes in energy substrate supply. Given the high flux of energy substrates and the centrality of their appropriate use for optimal cardiac function, it is not surprising that the heart has intricate signaling mechanisms through which it responds to metabolic stress. This review focuses on the changes in gene expression in myocardial and vascular tissues during metabolic stress that affect mRNAs and subsequent protein synthesis with an eye toward understanding the manner in which these changes effect adaptive and maladaptive responses of the heart. This article is part of a Special Issue entitled "Focus on Cardiac Metabolism".
- Diabetic cardiomyopathy
- Histone deacetylation
- Nuclear receptor transcription factor
- Pathological hypertrophy
- Protein translation