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Notably, embryonic cardiomyocytes lacking LONP1 exhibit accumulation of abnormal mitochondrial protein aggregates, which subsequently activate the phosphorylation of eukaryotic initiation factor 2 (eIF2)-transcription factor 4 (ATF4) signaling axis to trigger compensatory metabolic remodeling: ATF4 upregulates the expression of glucose transporter 1 (GLUT1) to enhance glycolytic energy production

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