title: Linking gene expression to function: metabolic flexibility in the normal and diseased heart.
abstract: 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.
authors.affiliation: Division of Cardiology, Department of Internal Medicine, University of Texas Houston Medical School, 6431 Fannin, MSB 1.246 Houston, TX 77030, USA. heinrich.taegtmeyer@uth.tmc.edu
authors.forename: Heinrich
authors.initials: H
authors.lastname: Taegtmeyer
authors.forename: Leonard
authors.initials: L
authors.lastname: Golfman
authors.forename: Saumya
authors.initials: S
authors.lastname: Sharma
authors.forename: Peter
authors.initials: P
authors.lastname: Razeghi
authors.forename: Melissa
authors.initials: M
authors.lastname: van Arsdall
mesh_terms: D003920:Diabetes Mellitus / Q000378:metabolism / Q000503:physiopathology; D015870:Gene Expression; D006801:Humans; D009206:Myocardium / Q000378:metabolism*; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D018160:Receptors, Cytoplasmic and Nuclear; D014157:Transcription Factors