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Maintenance of mitochondrial function is crucial, especially for the energy-demanding and metabolically active neuronal cells. Owing to their post-mitotic nature, neurons are highly vulnerable to mitochondrial dysfunction and therefore rely heavily on mitochondrial quality control mechanisms to mitigate damage and sustain cellular and organismal homeostasis. Mitophagy, the selective autophagic degradation of mitochondria, is the prominent mitochondrial turnover mechanism, required for supporting proper neuronal development and function.
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Ploumi et al. (2025) studied this question.
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