Arsenic trioxide-induced acute kidney injury: OPA1- and Drp1-mediated mitochondrial dynamics imbalance, PINK1/Parkin-dependent mitophagy, and Chuanhuang Fang III.

ABSTRACT:

Purpose

Acute kidney injury (AKI) remains a global health concern with limited therapies. Among its causes, arsenic (AS)-induced AKI (AI-AKI), exemplified by the antitumor agent arsenic trioxide (ATO), represents an emerging clinical challenge. Despite its clinical efficacy in treating AI-AKI, the protective mechanism of Chuanhuang Fang III (CHF) remains unclear. This study aimed to investigate the mechanisms and therapeutic targets of CHF against AI-AKI.

Methods

Classic AI-AKI rat model was established, and subsequently treated with graded doses of CHF. CHF constituents were identified. Renal pathology, renal function, and AKI biomarkers were detected. Mitochondrial quality control-related parameters were detected as follows: 1) transmission electron microscopy was employed

SUBMITTER: Wang P 

PROVIDER: S-EPMC12900759 | biostudies-literature | 2026

REPOSITORIES: biostudies-literature