ArticleTranslational pediatrics2026
PTEN modulates mitochondrial dysfunction in podocytes via the PINK1/Parkin signal pathway.
Article in Translational pediatrics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Mitochondrial dysfunction and impaired autophagy in podocytes contribute to the pathogenesis of kidney diseases, and the phosphatase and tensin homolog (PTEN)-PTEN-induced putative kinase 1 (PINK1)/Parkin signaling axis has emerged as a critical regulator of mitochondrial quality control and podocyte survival; however, the precise underlying mechanisms remain unclear. This study investigates how the PTEN-PINK1/Parkin axis governs mitochondrial quality control in podocytes. Methods: Results: PTEN depletion markedly suppressed PINK1 accumulation, leading to attenuated Parkin recruitment and LC3-I to LC3-II conversion. This defect correlated with defective clearance of depolarized mitochondria and exacerbated organelle damage. Conversely, PTEN upregulation potentiated PINK1 stabilization, enhanced Parkin translocation to mitochondria, and promoted LC3-II-mediated autophagosome formation, collectively restoring mitophagic autophagosome formation. Conclusions: Podocyte-specific PTEN overexpression confers protection against glomerular podocyte injury by mitigating mitophagy dysfunction via the PTEN-PINK1/Parkin signal pathway, highlighting a potential therapeutic target for glomerular diseases.
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