Alisson C Cardoso1, Ana Helena M Pereira1, Hesham A Sadek2,3. 1. Brazilian Biosciences National Laboratory, Brazilian Center for Research in Energy and Materials (CNPEM), Campinas, Sao Paulo, Brazil. 2. Department of Internal Medicine, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX, 75390, USA. hesham.sadek@utsouthwestern.edu. 3. Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA. hesham.sadek@utsouthwestern.edu.
Abstract
PURPOSE OF REVIEW: This review provides an overview of the molecular mechanisms underpinning the cardiac regenerative capacity during the neonatal period and the potential targets for developing novel therapies to restore myocardial loss. RECENT FINDINGS: We present recent advances in the understanding of the molecular mechanisms of neonatal cardiac regeneration and the implications for the development of new cardiac regenerative therapies. During the early postnatal period, several cell types and pathways are involved in cardiomyocyte proliferation including immune response, nerve signaling, extracellular matrix, mitochondria substrate utilization, gene expression, miRNAs, and cell cycle progression. The early neonatal mammalian heart has remarkable regenerative capacity, which is mediated by proliferation of endogenous cardiomyocytes, and is lost when cardiomyocytes stop dividing shortly after birth. A wide array of mechanisms that regulate this regenerative process have been proposed.
PURPOSE OF REVIEW: This review provides an overview of the molecular mechanisms underpinning the cardiac regenerative capacity during the neonatal period and the potential targets for developing novel therapies to restore myocardial loss. RECENT FINDINGS: We present recent advances in the understanding of the molecular mechanisms of neonatal cardiac regeneration and the implications for the development of new cardiac regenerative therapies. During the early postnatal period, several cell types and pathways are involved in cardiomyocyte proliferation including immune response, nerve signaling, extracellular matrix, mitochondria substrate utilization, gene expression, miRNAs, and cell cycle progression. The early neonatal mammalian heart has remarkable regenerative capacity, which is mediated by proliferation of endogenous cardiomyocytes, and is lost when cardiomyocytes stop dividing shortly after birth. A wide array of mechanisms that regulate this regenerative process have been proposed.
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