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. 2021 Apr 28;8:647785. doi: 10.3389/fcvm.2021.647785

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Copyright © 2021 Pluijmert, Atsma and Quax.

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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Innate immunity following myocardial ischemia–reperfusion injury. Ischemic-induced myocardial cell death activates innate immunity. Expression of endogenous ligands upon reperfusion are known as danger-associated molecular patterns (DAMPs) including HMGB1, high-mobility group box-1; HSPs, heat shock proteins; OSEs, oxidation-specific epitopes; HA, hyaluronic acid. These DAMPs are recognized by pattern recognition receptors (PRRs) like TLRs, NLRs, RAGE, complement cascade, reactive oxygen species (ROS), and chemoattractants. Finally, activation of the nuclear factor (NF)-κB and mitogen-activated protein kinase (MAPK) pathways induce the expression of pro-inflammatory chemokines, cytokines, and adhesion molecules regulating a complex post-ischemic inflammatory response.