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. 2020 Oct 30;7:588206. doi: 10.3389/fcvm.2020.588206

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Copyright © 2020 Wang, Ge, Chen, Mao and Zhu.

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 mechanism of gaseous signaling molecules (NO, H₂, H₂S) against myocardial ischemic injury H₂S, hydrogen sulfide; GSK3β, Glycogen synthase kinase-3β; GP130, Glycoprotein 130;STAT3, Signal transducers and activators of transcription 3; PI3K, class I phosphatidylinositol 3-kinase; COX2, Cyclooxygenase 2; AKT, Serine/threonine protein kinase; MAPK, mitogen-activated protein kinase; cGMP, cyclic guanosinc monophosphate; NO, nitric oxide; i-NOS, Inducible nitric oxide synthase; e-NOS, endothelial nitric oxide synthase; Keap1, Kelch Like ECH Associated Protein 1; Nrf2, Nuclear factor erythroid 2 p45-related factor 2; NF-kB, Nuclear factor-kappa B; HO-1, Hemeoxygenase-1; SIRT1, Sirtuin1; ROS, Reactive oxygen species.