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. 2019 Oct 25;6:150. doi: 10.3389/fcvm.2019.00150

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Copyright © 2019 Harhous, Booz, Ovize, Bidaux and Kurdi.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The involvement of STAT3 in the regulation of ER activity. STAT3 decreases cellular death under different conditions through its ER-dependent activity. Following I/R, JAK2-STAT3 pathway rescues SERCA expression and activity, which reduces the ER stress occurring during I/R injury. This reduces cell death and helps in inducing the infarct size. In addition, STAT3 modulates the ER-mitochondrial calcium release by directly interacting with IP3R3 and facilitating its degradation. This consequently leads to a decrease in the calcium release from ER to mitochondria, and thus causes a decrease in apoptotic cell death. The S727 STAT3 residue plays a regulatory role. The images of ER and mitochondria were adapted from Servier Medical Art (https://smart.servier.com/).