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Editorial
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This editorial introduces a special issue focused on metabolic remodeling in heart failure, highlighting the shift towards understanding metabolic mechanisms alongside structural changes.
This editorial refers to a collection of nine review articles invited for this special issue on metabolic remodelling in heart failure, guest edited by Torsten Doenst and E. Dale Abel The term ‘remodelling’ has been abundantly used in the context of heart failure with many different meanings.1–3 It was originally described in a rat model as the structural and functional response of the remote heart muscle to a local infarct caused by the occlusion of the left anterior descending coronary artery.4 Thereafter, a plethora of experimental and clinical studies have addressed mechanisms of remodelling and the concept is widely linked to the development of heart failure.5 However, metabolic aspects of remodelling have until recently been less well investigated. The development of new molecular techniques, including diverse approaches to global analysis of gene expression6,7 and broad-based approaches such as proteomics and metabolomics8–10 has provided a wealth of new information on underlying mechanisms. However, the information derived from these techniques represent a ‘snapshot’ of a functional continuum because they require tissue samples which are usually derived from a specific time point. Although these approaches have proved to be extemely valuable, the functional relevance of many findings is not always obvious. For example, there has been a resurgence in the use of classic metabolic approaches such as assessing rates of substrate utilization, enzyme activities, and ATP synthesis rates. In the heart failure field, these developments are specifically important since changes in contractile function are associated with changes in energy demand (i.e. the processes involved in energy production and conversion).
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Doenst et al. (2011) studied this question.
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