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ABSTRACT: Purpose
Sepsis-induced acute kidney injury (S-AKI) is a severe complication of sepsis. This study aimed to explore the protective effects of Maresin-1 (MaR-1) on S-AKI and elucidate its potential molecular mechanisms, focusing on ferroptosis and the Nrf2/HO-1/GPx4 signaling pathway.Methods
In vitro cellular experiments and in vivo mouse models of S-AKI were employed. Cell viability, ferroptosis-related markers (reactive oxygen species [ROS], malondialdehyde [MDA], and iron ion concentration), and antioxidant protein expression were analyzed. The Nrf2/HO-1/GPx4 signaling pathway was examined using Western blotting. In vivo, renal injury markers (blood urea nitrogen [BUN], serum creatinine [SCr], and neutrophil gelatinase-associated lipocalin [NGAL]) and
SUBMITTER: Tang L
PROVIDER: S-EPMC12570256 | biostudies-literature | 2025 Dec
REPOSITORIES: biostudies-literature