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While mitophagy serves as a critical quality control mechanism by eliminating mitochondria impaired by OS and maintaining alveolar development, extensive evidence shows that excessive activation (such as through the CerS1/Drp1-dependent ceramide pathway) or functional defects (such as lysosomal metabolic abnormalities mediated by GBA1) can induce cell death across various disease conditions (Oleinik et al., 2023

This paradigm-shifting discovery may prove foundational for developing tissue-selective therapeutic strategies targeting these acquired molecular vulnerabilities

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