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Linking Gene Expression to Function: Metabolic Flexibility in the Normal and Diseased Heart
HEINRICH TAEGTMEYER,
LEONARD GOLFMAN,
SAUMYA SHARMA,
PETER RAZEGHI AND
MELISSA VAN ARSDALL
Division of Cardiology, Department of Internal Medicine, The University of Texas Houston Medical School, Houston, Texas 77030, USA
Address for correspondence: Heinrich Taegtmeyer, M.D., D.Phil., University of Texas Houston Medical School, Department of Internal Medicine, Division of Cardiology, 6431 Fannin, MSB 1.246 Houston, TX 77030. Fax: 713-500-6556. heinrich.taegtmeyer{at}uth.tmc.edu
Ann. N.Y. Acad. Sci. 1015: 203-214 (2004).
Metabolism transfers energy from substrates to ATP. As a "metabolic omnivore," the normal heart adapts to changes in the environment by switching from one substrate to another. We propose that this flexibility is lost in the maladapted, diseased heart. Both adaptation and maladaptation are the results of metabolic signals that regulate transcription of key cardiac regulatory genes. We propose that metabolic remodeling precedes, initiates, and sustains functional and structural remodeling. The process of metabolic remodeling then becomes a target for pharmacological intervention restoring metabolic flexibility and normal contractile function of the heart.
Key Words: energy metabolism • gene expression • hypoxia • diabetes • heart failure
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