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• W2166444451 abstract "Because apoptotic death plays a critical role in cardiomyocyte loss during ischaemic heart injury, a detailed understanding of the mechanisms involved is likely to have a substantial impact on the optimization and development of treatment strategies. The goal of this study was to assess gene profiling during ischaemia/hypoxia and to evaluate the functions of ischaemia/hypoxia-responsive genes in in vivo and in vitro ischaemia/hypoxia-induced cardiomyocyte apoptosis models. DNA microarray analysis and real-time polymerase chain reaction were performed on hearts obtained from an in vivo rat transient ischaemia model and on neonatal rat cardiomyocytes from an in vitro hypoxia model. Three genes, namely Ddit4, Gadd45β and Atf3, were found to be up-regulated in vivo and in vitro. Using loss-of-function and gain-of-function techniques, the functions of these ischaemia/hypoxia-responsive genes were evaluated. Ischaemia/hypoxia-induced cardiomyocyte apoptosis was remarkably attenuated by the small interfering RNA-mediated down-regulation of Gadd45β in vivo and in vitro, whereas ectopic Gadd45β expression significantly aggravated hypoxia-induced apoptosis in vitro. These results suggest that Gadd45β is a key player in ischaemia/hypoxia-induced apoptotic cardiomyocyte death, and that strategies based on its inhibition might be of benefit in the treatment of acute ischaemic heart disease." @default.
• W2166444451 created "2016-06-24" @default.
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• W2166444451 date "2010-02-12" @default.
• W2166444451 modified "2023-09-30" @default.
• W2166444451 title "Gadd45 is a novel mediator of cardiomyocyte apoptosis induced by ischaemia/hypoxia" @default.
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• W2166444451 doi "https://doi.org/10.1093/cvr/cvq048" @default.
• W2166444451 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20154065" @default.
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