MTOR Inhibition limits LPS induced acute kidney injury and ameliorates hallmarks of cellular senescence.

ABSTRACT: Sepsis-induced acute kidney injury (AKI) can lead to chronic renal dysfunction with accelerated renal aging. Activation of the mammalian target of rapamycin (mTOR) is implicated in the initiation and progression of renal injury. This study investigates the effectiveness of the mTOR inhibitor, rapamycin, in mitigating kidney injury and explores the underlying mechanisms. AKI was induced by intraperitoneal administration of a solution containing 10 mg/kg of lipopolysaccharide (LPS) in a mouse model. Two groups of endotoxemic mice received pre- and post- treatment with rapamycin. Whole-genome DNA methylation analysis was performed on renal proximal tubular epithelial cells (RPTEC). In the LPS-induced AKI mouse model, rapamycin treatment significantly reduced creatinine levels, preserved renal

SUBMITTER: Stasi A 

PROVIDER: S-EPMC11926175 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature