Redox DAPK1 destabilizes Pellino1 to govern inflammation-coupling tubular damage during septic AKI

作者：Bangchuan Hu, Guohua Wu, Ziqiang Shao, Zheng Yang, Jinquan Liu, Run Zhang, Jun Ki Hong, Xianghong Yang, Ren-Hua Sun, Shi‐Jing Mo · 发表于：Theranostics · 年份：2020 · DOI：10.7150/thno.49870 · 被引用次数：26 · 研究领域：Acute Kidney Injury Research、Neutrophil, Myeloperoxidase and Oxidative Mechanisms、Advanced Glycation End Products research

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.