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Ann N Y Acad Sci. 2010 Feb;1188:191-8. doi: 10.1111/j.1749-6632.2009.05100.x.

Return to the fetal gene program: a suggested metabolic link to gene expression in the heart.

Author information

1
The University of Texas-Houston Medical School, Department of Internal Medicine, Division of Cardiology, Houston, Texas 77030, USA. Heinrich.Taegtmeyer@uth.tmc.edu

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.

PMID:
20201903
PMCID:
PMC3625436
DOI:
10.1111/j.1749-6632.2009.05100.x
[Indexed for MEDLINE]
Free PMC Article

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