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• W2893143399 abstract "To explore the underlying mechanisms of Hrd1/sema3a/IGF-1R on cardiomyocyte apoptosis. AMI model was established by the left-anterior descending coronary artery (LAD) ligation. The expressions of Hrd1, sema3a and IGF-1R were examined by western blot. The activity of caspase-3 and caspase-8 was measured using the corresponding activity detection kit. Cardiomyocyte apoptosis was detected by flow cytometry assay. Co-immunoprecipitation and ubiquitination assay were used to test the relationship among Hrd1, sema3a and IGF-1R. Hrd1 expression and the activity of caspase-3 and caspase-8 were increased in cardiac tissues of AMI rats and hypoxia-induced cardiomyocytes, while IGF-1R expression was decreased. Hrd1 overexpression promoted IGF-1R degradation, whereas knockdown of sema3a suppressed this degradation. Moreover, knockdown of Hrd1 or sema3a could inhibit the decrease of IGF-1R expression induced by hypoxia, and reverse the enhanced activity of caspase-3 and caspase-8 and the increase of cardiomyocytes apoptosis induced by hypoxia, while si-IGF-1R countered these effects. In AMI rat experiments, interfering Hrd1 or sema3a reduced the infarct size and increased IGF-1R expression, but these could be abolished by si-IGF-1R. Hrd1 might mediate the ubiquitination of IGF-1R through sema3a and then participate in the regulation of cardiomyocyte apoptosis." @default.
• W2893143399 created "2018-10-05" @default.
• W2893143399 creator A5006900383 @default.
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• W2893143399 date "2018-12-01" @default.
• W2893143399 modified "2023-10-15" @default.
• W2893143399 title "Hrd1 induces cardiomyocyte apoptosis via regulating the degradation of IGF-1R by sema3a" @default.
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• W2893143399 doi "https://doi.org/10.1016/j.bbadis.2018.09.020" @default.
• W2893143399 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30248386" @default.
• W2893143399 hasPublicationYear "2018" @default.
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