Dexmedetomidine alleviates sepsis-associated acute kidney injury by inhibiting renal tubular ferroptosis via JNK/MAPK-LCN2 pathway.

ABSTRACT:

Background

Sepsis-associated acute kidney injury (SA-AKI), one of the most common complications of sepsis, significantly prolongs hospitalization, increases mortality, and elevates risks of cardiovascular events and chronic kidney disease. Critically, there are insufficient effective and safe clinical treatment drugs for SA-AKI, and new therapeutic strategies urgently need to be explored. Dexmedetomidine (Dex), a clinically widely used, highly selective α2-adrenoceptor agonist, exhibits sedative, analgesic, anxiolytic, sympatholytic, and opioid-sparing properties. Although recent clinical studies demonstrate its protective effects against SA-AKI, Dex's mechanisms of action remain incompletely understood and require further elucidation.

Methods

We performed RNA sequencing on

SUBMITTER: Liu B 

PROVIDER: S-EPMC12914927 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature