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Return to the Fetal Gene Program: a Suggested Metabolic Link to Gene Expression in the Heart

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Specialty Science
Date 2010 Mar 6
PMID 20201903
Citations 211
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Abstract

A hallmark of cardiac metabolism before birth is the predominance of carbohydrate use for energy provision. After birth, energy substrate metabolism rapidly switches to the oxidation of fatty acids. This switch accompanies the expression of "adult" isoforms of metabolic enzymes and other proteins. However, in a variety of pathophysiologic conditions, including hypoxia, ischemia, hypertrophy, atrophy, diabetes, and hypothyroidism, the postnatal heart returns to the "fetal" gene program. These adaptive mechanisms are also a feature of the failing heart muscle, where at a certain point this fetal-like reprogramming no longer suffices to support cardiac structure and function. We advance the hypothesis that in the postnatal heart, metabolic remodeling triggers the process through glycosylation of transcription factors, potentially protecting the stressed heart from irreversible functional impairment and programmed cell death. In other words, we propose a metabolic link to gene expression in the heart.

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References
1.
Chess D, Stanley W . Role of diet and fuel overabundance in the development and progression of heart failure. Cardiovasc Res. 2008; 79(2):269-78. DOI: 10.1093/cvr/cvn074. View

2.
Matsui T, Nagoshi T, Rosenzweig A . Akt and PI 3-kinase signaling in cardiomyocyte hypertrophy and survival. Cell Cycle. 2003; 2(3):220-3. View

3.
Razeghi P, Young M, Abbasi S, Taegtmeyer H . Hypoxia in vivo decreases peroxisome proliferator-activated receptor alpha-regulated gene expression in rat heart. Biochem Biophys Res Commun. 2001; 287(1):5-10. DOI: 10.1006/bbrc.2001.5541. View

4.
Smith R . Parturition. N Engl J Med. 2007; 356(3):271-83. DOI: 10.1056/NEJMra061360. View

5.
Kurabayashi M, Tsuchimochi H, Komuro I, Takaku F, Yazaki Y . Molecular cloning and characterization of human cardiac alpha- and beta-form myosin heavy chain complementary DNA clones. Regulation of expression during development and pressure overload in human atrium. J Clin Invest. 1988; 82(2):524-31. PMC: 303543. DOI: 10.1172/JCI113627. View