<i>In vitro</i> experiments using the HK-2 cell line provided further evidence supporting the <i>in vivo</i> findings.<h4>Conclusion</h4>The pathogenesis of clinical-dose ATO-induced AKI involves OPA1- and Drp1-mediated mitochondrial dynamics imbalance and PINK1/Parkin-dependent mitophagy in renal tubular epithelial cells, CHF ameliorated this injury by restoring mitochondrial quality control, highlighting its therapeutic potential against AI-AKI. The gene discussed is OPA1; the disease is congestive heart failure.