Heart failure is a leading cause of morbidity and mortality worldwide, currently affecting 5 million Americans. A syndrome defined on clinical terms, heart failure is the end result of events occurring in multiple heart diseases, including hypertension, myocardial infarction, genetic mutations and diabetes, and metabolic dysregulation, is a hallmark feature. Mounting evidence from clinical and preclinical studies suggests strongly that fatty acid uptake and oxidation are adversely affected, especially in end-stage heart failure. Moreover, metabolic flexibility, the heart's ability to move freely among diverse energy substrates, is impaired in heart failure. Indeed, impairment of the heart's ability to adapt to its metabolic milieu and associated metabolic derangement are important contributing factors in the heart failure pathogenesis. Elucidation of molecular mechanisms governing metabolic control in heart failure will provide critical insights into disease initiation and progression, raising the prospect of advances with clinical relevance.
*Department of Internal Medicine, Division of Cardiology, University of Texas Southwestern Medical Center, Dallas, TX; and
†Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX.
Reprints: Joseph A. Hill, MD, PhD, Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, NB11.200, 6000 Harry Hines Boulevard, Dallas, TX 75390-8573 (e-mail: email@example.com).
Supported by grants from the National Institutes of Health (HL-080144, HL-0980842, and HL-100401), Cancer Prevention and Research Institute of Texas CPRIT (CPRIT, RP110486P3), the AHA DeHaan Foundation (0970518N), and the Fondation Leducq (11CVD04). Zhao V. Wang was supported by a postdoctoral fellowship from the AHA (10POST4320009).
The authors report no conflicts of interest.
Received July 07, 2013
Accepted November 21, 2013