Journal of Inflammation Research, Год журнала: 2024, Номер Volume 17, С. 9485 - 9505

Опубликована: Ноя. 1, 2024

Sepsis-associated acute kidney injury (S-AKI) is a prevalent and severe clinical complication in intensive care units (ICUs) associated with high mortality poor prognosis. The dysfunction of renal tubular epithelial cells (TECs), particularly through their metabolic reprogramming, plays critical role the onset progression S-AKI. CITED2 shown to regulate variety cellular processes, but its specific impact on TECs metabolism S-AKI pathogenesis remains unclear. aim this study was investigate reprogramming effects inflammation C57BL/6 mouse model established using cecal ligation puncture (CLP). We assessed inflammatory responses, glucose expression kidneys septic mice. Additionally, effect evaluated vivo vitro models. silencing overexpression were employed elucidate regulatory role, focusing AKT signaling pathway. causes structural functional damage, aggravated dysregulated metabolism, accompanied by increased CITED2. attenuated reduced inflammation, thereby protecting from injury. Conversely, exacerbated dysfunction, promoted worsened Mechanistically, regulates TEC pathway, promoting S-AKI-related contributing drives aggravating response leading injury, highlighting Targeting inhibition may represent novel therapeutic approach for managing

Язык: Английский