Renoprotective Effects of MIT-001 in Ischemia-Reperfusion Injury: Modulation of Ferroptosis, ROS and Fibrotic Markers.

ABSTRACT: Renal ischemia-reperfusion injury (IRI) is a key driver of the progression from acute kidney injury (AKI) to chronic kidney disease (CKD), primarily through mechanisms involving oxidative stress, ferroptosis, and inflammation that promote fibrotic remodelling. This study investigates the therapeutic potential of MIT-001, a mitochondria-targeted reactive oxygen species (ROS) scavenger, in mitigating renal IRI. In vitro, MIT-001 attenuated ferroptotic cell death and fibrotic responses in HK-2 cells challenged with TGF-β or RSL3. MIT-001 restored GPX4 expression and activity, activated Nrf2 signalling, reduced lipid ROS and suppressed fibrogenic markers (α-SMA, Snail, collagen IV), while preserving E-cadherin levels. In a bilateral renal IRI mouse model, administration of MIT-001 significantl

SUBMITTER: Shin JA 

PROVIDER: S-EPMC12544698 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature