Targeting CDC42 Protects Mitochondrial Function through KLF2/HIF-1α/PINK1 Signaling in Acute Kidney Injury.

ABSTRACT: Acute kidney injury (AKI) is a severe clinical syndrome strongly associated with mitochondrial dysfunction and oxidative stress, yet effective therapies remain elusive. Here, we identify cell division cycle 42 (CDC42) as a critical mediator of AKI. Analysis of human single-cell RNA sequencing (scRNA-seq) dataset revealed marked upregulation of CDC42 in renal tubular epithelial cells (RTECs), which was validated in murine models of cisplatin- and ischemia-reperfusion-induced AKI. Pharmacological inhibition, conditional knockdown, or genetic ablation of CDC42 significantly alleviated renal injury, preserved mitochondrial function, and reduced reactive oxygen species (ROS) both in vivo and in vitro. Mechanistically, transcriptomic analysis, bioinformatic analysis, dual-luciferas

SUBMITTER: Zhou X 

PROVIDER: S-EPMC12837847 | biostudies-literature | 2026

REPOSITORIES: biostudies-literature