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. 2021 Jun 11;9:693262. doi: 10.3389/fcell.2021.693262

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Copyright © 2021 Zhang, Zhu, Miao and Liang.

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 S100A11 in TNF-α, CXCLs, and IL-1β induced inflammation. TNF-α, CXCL8, and IL-1β induce the expression of S100A11. Subsequently, S100A11 is secreted through a Caspase-1 dependent manner. Extracellular S100A11 is dimerized under the catalysis of TG2, and then binds to the RAGE receptor to induce the expression of inflammatory genes through the p38 MAPK signaling pathway, which causes inflammation progression. CXCLs, CXC chemokine ligands; TG2, transglutaminase 2. The circled “P” represents phosphorylation.