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By inhibiting lipid ROS generation and the hyperpolarization of mitochondrial membrane potential, mitoglitazone could restore mitochondrial DNA copy number, the generation of ATP, and mitochondrial morphology in kidney tissue, inhibiting mitochondrial dysfunction and ferroptosis induced by I/R

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EWS overexpression, however, promoted TERRA transcription only from telomeric sites 1q, 9p, 15q, and XqYq, and not 2q, 10q, 13q, 17p, and XpYp (Fig

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