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Cao T, Liccardo D, LaCanna R, et al. Fatty Acid Oxidation Promotes Cardiomyocyte Proliferation Rate but Does Not Change Cardiomyocyte Number in Infant Mice. Front Cell Dev Biol. 2019;7:42doi: 10.3389/fcell.2019.00042.
Cao, T., Liccardo, D., LaCanna, R., Zhang, X., Lu, R., Finck, B. N., Leigh, T., Chen, X., Drosatos, K., & Tian, Y. (2019). Fatty Acid Oxidation Promotes Cardiomyocyte Proliferation Rate but Does Not Change Cardiomyocyte Number in Infant Mice. Frontiers in cell and developmental biology, 742. https://doi.org/10.3389/fcell.2019.00042
Cao, Tongtong, et al. "Fatty Acid Oxidation Promotes Cardiomyocyte Proliferation Rate but Does Not Change Cardiomyocyte Number in Infant Mice." Frontiers in cell and developmental biology vol. 7 (2019): 42. doi: https://doi.org/10.3389/fcell.2019.00042
Cao T, Liccardo D, LaCanna R, Zhang X, Lu R, Finck BN, Leigh T, Chen X, Drosatos K, Tian Y. Fatty Acid Oxidation Promotes Cardiomyocyte Proliferation Rate but Does Not Change Cardiomyocyte Number in Infant Mice. Front Cell Dev Biol. 2019 Mar 22;7:42. doi: 10.3389/fcell.2019.00042. eCollection 2019. PMID: 30968022; PMCID: PMC6440456.
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Front Cell Dev Biol. 2019 Mar 22;7:42. doi: 10.3389/fcell.2019.00042. eCollection 2019.

Fatty Acid Oxidation Promotes Cardiomyocyte Proliferation Rate but Does Not Change Cardiomyocyte Number in Infant Mice.

Frontiers in cell and developmental biology

Tongtong Cao, Daniela Liccardo, Ryan LaCanna, Xiaoying Zhang, Rong Lu, Brian N Finck, Tani Leigh, Xiongwen Chen, Konstantinos Drosatos, Ying Tian

Affiliations

  1. Department of Pharmacology, Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, United States.
  2. Department of Pathology, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
  3. Department of Physiology, Cardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, United States.
  4. Division of Geriatrics and Nutritional Sciences, Department of Medicine, Washington University School of Medicine in St. Louis, St. Louis, MO, United States.

PMID: 30968022 PMCID: PMC6440456 DOI: 10.3389/fcell.2019.00042

Abstract

Cardiomyocyte proliferation accounts for the increase of cardiac muscle during fetal mammalian heart development. Shortly after birth, cardiomyocyte transits from hyperplasia to hypertrophic growth. Here, we have investigated the role of fatty acid β-oxidation in cardiomyocyte proliferation and hypertrophic growth during early postnatal life in mice. A transient wave of increased cell cycle activity of cardiomyocyte was observed between postnatal day 3 and 5, that proceeded as cardiomyocyte hypertrophic growth and maturation. Assessment of cardiomyocyte metabolism in neonatal mouse heart revealed a myocardial metabolic shift from glycolysis to fatty acid β-oxidation that coincided with the burst of cardiomyocyte cell cycle reactivation and hypertrophic growth. Inhibition of fatty acid β-oxidation metabolism in infant mouse heart delayed cardiomyocyte cell cycle exit, hypertrophic growth and maturation. By contrast, pharmacologic and genetic activation of PPARα, a major regulator of cardiac fatty acid metabolism, induced fatty acid β-oxidation and initially promoted cardiomyocyte proliferation rate in infant mice. As the cell cycle proceeded, activation of PPARα-mediated fatty acid β-oxidation promoted cardiomyocytes hypertrophic growth and maturation, which led to cell cycle exit. As a consequence, activation of PPARα-mediated fatty acid β-oxidation did not alter the total number of cardiomyocytes in infant mice. These findings indicate a unique role of fatty acid β-oxidation in regulating cardiomyocyte proliferation and hypertrophic growth in infant mice.

Keywords: cardiomyocyte; fatty acid oxidation; hypertrophic growth; infant mice; proliferation

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