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Under pathological conditions characterized by deficient mitophagy, pharmacological agents such as rapamycin or aai berry restore mitochondrial turnover, thereby promoting apoptosis and reducing angiogenesis in lesions reliant on AKT/mTOR signaling (6668)

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In renal tubular epithelial cells (RTECs), knockdown of NCOA4 could ameliorate ferroptosis caused by the activation of autophagy[23]

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