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Can the cardiomyocyte cell cycle be reprogrammed?

Bicknell, K.A., Coxon, C.N.H. and Brooks, G. (2007) Can the cardiomyocyte cell cycle be reprogrammed? Journal of Molecular and Cellular Cardiology, 42 (4). pp. 706-721. ISSN 0022-2828

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To link to this article DOI: 10.1016/j.yjmcc.2007.01.006

Abstract/Summary

Cardiac repair following myocardial injury is restricted due to the limited proliferative potential of adult cardiomyocytes. The ability of mammalian cardiomyocytes to proliferate is lost shortly after birth as cardiomyocytes withdraw from the cell cycle and differentiate. We do not fully understand the molecular and cellular mechanisms that regulate this cell cycle withdrawal, although if we could it might lead to the discovery of novel therapeutic targets for improving cardiac repair following myocardial injury. For the last decade, researchers have investigated cardiomyocyte cell cycle control, commonly using transgenic mouse models or recombinant adenoviruses to manipulate cell cycle regulators in vivo or in vitro. This review discusses cardiomyocyte cell cycle regulation and summarises recent data from studies manipulating the expressions and activities of cell cycle regulators in cardiomyocytes. The validity of therapeutic strategies that aim to reinstate the proliferative potential of cardiomyocytes to improve myocardial repair following injury will be discussed. (c) 2007 Elsevier Inc. All rights reserved.

Item Type:Article
Refereed:Yes
Divisions:Faculty of Life Sciences > School of Chemistry, Food and Pharmacy > School of Pharmacy
Interdisciplinary centres and themes > Institute for Cardiovascular and Metabolic Research (ICMR)
ID Code:13785
Uncontrolled Keywords:cardiomyocyte, cell cycle, cell division, cyclins, cyclin dependent, kinases, E2F, mitosis, p38 MAPK, regeneration, ACTIVATED PROTEIN-KINASE, CARDIAC MYOCYTE HYPERTROPHY, RAT VENTRICULAR, MYOCYTES, C-MYC PROTOONCOGENE, MITOSIS-SPECIFIC PHOSPHORYLATION, MITOTIC CHROMOSOME CONDENSATION, MYOCARDIUM IN-VIVO, DNA-SYNTHESIS, HISTONE H3, GENE-TRANSCRIPTION

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