Diseases 2017, 5(2), 14; doi:10.3390/diseases5020014
Targeting Metabolic Modulation and Mitochondrial Dysfunction in the Treatment of Heart Failure
1
School of Medicine, Flinders University, Adelaide 5042, Australia
2
Division of Molecular and Clinical Medicine, Mailbox 2, Ninewells Hospital and Medical School, University of Dundee, Dundee DD1 9SY, UK
*
Author to whom correspondence should be addressed.
Academic Editor: Maurizio Battino
Received: 25 February 2017 / Revised: 21 April 2017 / Accepted: 27 April 2017 / Published: 10 May 2017
(This article belongs to the Special Issue Current and Potential Therapeutic Strategies for Heart Failure)
Abstract
Despite significant improvements in morbidity and mortality with current evidence-based pharmaceutical-based treatment of heart failure (HF) over the previous decades, the burden of HF remains high. An alternative approach is currently being developed, which targets myocardial energy efficiency and the dysfunction of the cardiac mitochondria. Emerging evidence suggests that the insufficient availability of ATP to the failing myocardium can be attributed to abnormalities in the myocardial utilisation of its substrates rather than an overall lack of substrate availability. Therefore, the development of potential metabolic therapeutics has commenced including trimetazidine, ranolazine and perhexiline, as well as specific mitochondrial-targeting pharmaceuticals, such as elamipretide. Large randomised controlled trials are required to confirm the role of metabolic-modulating drugs in the treatment of heart failure, but early studies have been promising in their possible efficacy for the management of heart failure in the future. View Full-TextKeywords:
heart failure; metabolic; mitochondria; trimetazidine; ranolazine; perhexiline; elamipretide
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Steggall, A.; Mordi, I.R.; Lang, C.C. Targeting Metabolic Modulation and Mitochondrial Dysfunction in the Treatment of Heart Failure. Diseases 2017, 5, 14.
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