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Review

Molecular Control of Cardiac Fetal/Neonatal Remodeling

Division of Medicine, University College London, London WC1 E6JJ, UK
J. Cardiovasc. Dev. Dis. 2014, 1(1), 29-36; https://doi.org/10.3390/jcdd1010029
Received: 19 December 2013 / Revised: 19 March 2014 / Accepted: 21 March 2014 / Published: 26 March 2014
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. View Full-Text
Keywords: cardiac; neonatal; metabolism; HIF; PPAR cardiac; neonatal; metabolism; HIF; PPAR
MDPI and ACS Style

Breckenridge, R.A. Molecular Control of Cardiac Fetal/Neonatal Remodeling. J. Cardiovasc. Dev. Dis. 2014, 1, 29-36. https://doi.org/10.3390/jcdd1010029

AMA Style

Breckenridge RA. Molecular Control of Cardiac Fetal/Neonatal Remodeling. Journal of Cardiovascular Development and Disease. 2014; 1(1):29-36. https://doi.org/10.3390/jcdd1010029

Chicago/Turabian Style

Breckenridge, Ross A. 2014. "Molecular Control of Cardiac Fetal/Neonatal Remodeling" Journal of Cardiovascular Development and Disease 1, no. 1: 29-36. https://doi.org/10.3390/jcdd1010029

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