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J. Cardiovasc. Dev. Dis. 2014, 1(1), 29-36; doi:10.3390/jcdd1010029
Review

Molecular Control of Cardiac Fetal/Neonatal Remodeling

Received: 19 December 2013; in revised form: 19 March 2014 / Accepted: 21 March 2014 / Published: 26 March 2014
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Abstract: Immediately following birth, the mammalian heart switches from generating ATP via glycolysis to β-oxidation of lipid. Coincident with this metabolic remodeling, cardiomyocyte mitosis ceases and regenerative capacity is lost. Recently, our understanding of the molecular pathways linking physiological stimuli with gene expression and phenotype changes around birth has increased, although fundamental gaps remain. This review discusses recent work that sheds light on this important area of mammalian cardiovascular development.
Keywords: cardiac; neonatal; metabolism; HIF; PPAR cardiac; neonatal; metabolism; HIF; PPAR
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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MDPI and ACS Style

Breckenridge, R.A. Molecular Control of Cardiac Fetal/Neonatal Remodeling. J. Cardiovasc. Dev. Dis. 2014, 1, 29-36.

AMA Style

Breckenridge RA. Molecular Control of Cardiac Fetal/Neonatal Remodeling. Journal of Cardiovascular Development and Disease. 2014; 1(1):29-36.

Chicago/Turabian Style

Breckenridge, Ross A. 2014. "Molecular Control of Cardiac Fetal/Neonatal Remodeling." J. Cardiovasc. Dev. Dis. 1, no. 1: 29-36.

J. Cardiovasc. Dev. Dis. EISSN 2308-3425 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert