Abstract
O ST E R A B ST R A C T S Results: In this study, we demonstrated that ER stress sensors, PERK (IRE1 (intositolrequiring enzyme-1) and ATF6, were activated in ROSmediated ER stressinduced cell apoptosis in rat model of DCM. We further showed that the deletion of PERK in cardiac cells exhibited stronger protective effect against apoptosis induced by highglucose incubation than deletion of ATF6 or IRE1 in the same cell line. By subcellular fractionation, rather than ATF6 and IRE1, in myocytes, PERK was found a component of MAMs which was the functional and physical contact site between ER and mitochondria. Conclusion: Thus, double sourced ROS stimulation makes PERK signaling pathway (PERKeIF2aATF4CHOP) take the major responsibility in ROSmediated ER stressinduced cell apoptosis in DCM. Disclosure of Interest: None Declared
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