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. 2015 Nov 16;5:16590. doi: 10.1038/srep16590

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Copyright © 2015, Macmillan Publishers Limited

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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CST acts as an endogenous M2 receptor agonist, activates M2 receptor and causes inhibition of adenylyl cyclase (AC) activity via the α subunit (αi) of Gi, thereby decreasing cAMP level while stimulating by isoproterenol or forskolin. During cardiac I/R, CST binds to M2 receptor and activates ERK1/2 and PI3 K/Akt signaling pathway to reduce ER-stress response and cell apoptosis.