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.
Wang et al. (Fri,) studied this question.
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