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. 2021 Apr 15;12:637753. doi: 10.3389/fimmu.2021.637753

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Copyright © 2021 Chen, Qiu, Yang, Zhang, Sun, Gao, Hei and Ji

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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LXA4 attenuates septic AKI via blocking crosstalk between inflammation and premature senescence in PPAR-γ-dependent manner. Sepsis would cause activation of NF-κB-mediated inflammation response and NF-κB/p53 mediated cellular premature senescence in kidney tissues. The inflammation response interplays with cellular premature senescence in septic AKI. Pretreatment with LXA4 promotes inflammation resolution and blocks the crosstalk between inflammation and premature senescence via PPAR-γ/NF-κB signaling.