Redox DAPK1 destabilizes Pellino1 to govern inflammation-coupling tubular damage during septic AKI
Bangchuan Hu, Guohua Wu, Ziqiang Shao, Zheng Yang, Jinquan Liu, Run Zhang, Jun Ki Hong, Xianghong Yang, Ren-Hua Sun, Shi‐Jing Mo
Abstract
Our findings provide a rationale for the mechanism whereby inflammation intersects with hypoxic tubular damage during septic AKI through a previously unappreciated role of DAPK1-inducible Ser39 phosphorylation in Pellino1 turnover and underscore that combined targeting DAPK1 and MyD88 might be a feasible strategy for septic AKI management.
Topics & Concepts
InflammationRedoxChemistryBiophysicsCell biologyMedicineBiologyImmunologyOrganic chemistryAcute Kidney Injury ResearchNeutrophil, Myeloperoxidase and Oxidative MechanismsAdvanced Glycation End Products research