PRDM16 suppresses ferroptosis to protect against sepsis-associated acute kidney injury by targeting the NRF2/GPX4 axis.

ABSTRACT: Acute kidney injury (AKI) constitutes a significant public health issue. Sepsis accounts for over 50 % of AKI cases in the ICU. Recent findings from our research indicated that the PRD1-BF1-RIZ1 homeodomain protein 16 (PRDM16) inhibited the progression of diabetic kidney disease (DKD). However, its precise role and regulatory mechanism in sepsis-induced AKI remain obscure. This study reveals that lipopolysaccharide (LPS) and cecum ligation and puncture (CLP) instigated PRDM16 expression in Boston University mouse proximal tubule (BUMPT) cells and mouse kidneys, respectively. Functionally, PRDM16 curtailed LPS-induced ferroptosis. Mechanistically, PRDM16 associates with the promoter regions of nuclear factor-erythroid 2-related factor-2 (NRF2) and augments its expression, subsequently enhan

SUBMITTER: Zheng Q 

PROVIDER: S-EPMC11612791 | biostudies-literature | 2024 Nov

REPOSITORIES: biostudies-literature