Transcriptomic analysis reveals mitophagy dysregulation in gestational diabetes, suggesting new therapeutic targets.
These findings suggest that mitophagy dysregulation is an early and persistent defect in GDM, with MUL1, PINK1, TOMM7, and ATF4 emerging as potential biomarkers and therapeutic targets. The results support the hypothesis that mitochondrial quality control failure contributes to the pathogenesis of GDM with similar patterns shown in both placental and cord blood tissues. However, these genes were not significantly altered in plasma, highlighting tissue context as a critical factor in detecting mitophagy-related dysregulation.
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Bouati et al. (2026) studied this question.
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