CD36 promotes tubular ferroptosis by regulating the ubiquitination of FSP1 in acute kidney injury.

ABSTRACT: Reactive oxidative species (ROS) production-driven ferroptosis plays a role in acute kidney injury (AKI). However, its exact molecular mechanism is poorly understood. Scavenger receptor CD36 has important roles in oxidizing lipids, lipid accumulation, metabolic syndrome, and insulin resistance in chronic kidney disease, but its roles remain unexplored in AKI. The present study investigated the role and mechanism of CD36 in regulating proximal tubular cell ferroptosis and AKI. The expression of CD36 was found to be significantly up-regulated in AKI renal tissues and correlated with renal function, which might serve as an independent biomarker for AKI patients. Moreover, in adult mice subjected to AKI, deletion of CD36 (CD36^-/-) induced tubular cell ROS accumulation, ferroptosis a

SUBMITTER: Ma Y 

PROVIDER: S-EPMC10425750 | biostudies-literature | 2024 Jan

REPOSITORIES: biostudies-literature