BMAL1 alleviates sepsis-induced AKI by inhibiting ferroptosis

The role of BMAL1 in various diseases remains unclear, particularly its impact on sepsis-induced acute kidney injury (AKI). This study aims to investigate the role of BMAL1 in sepsis-induced AKI and its potential effects on cell ferroptosis. Initially, we assessed BMAL1 expression levels in mice treated with sepsis-induced AKI (via LPS injection) and in LPS-stimulated renal tubular epithelial cells. Subsequently, we explored the correlation between BMAL1 and ferroptosis using sequencing technology, validating our findings throughout experimental approaches. To further elucidate BMAL1's specific effects on AKI-related ferroptosis, we constructed BMAL1 overexpression models in mice and cells, analysing its impact on AKI and ferroptosis both in vivo and in vitro. Furthermore, using transcriptome sequencing technology, we identified key BMAL1-regulated genes and their associated biological pathways, validating these findings through in vivo and in vitro experiments.