ArticleMedical science monitor : international medical journal of experimental and clinical research2019
PTEN-Induced Putative Kinase 1 (PINK1)/Parkin-Mediated Mitophagy Protects PC12 Cells Against Cisplatin-Induced Neurotoxicity.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Low-Level Laser Mitigates Cisplatin-Induced Oxidative Stress and Apoptosis via AMPK-Mediated Autophagy in PC12 Cells.ACS omega · 2026Article
- Role of the PKA-PGC1α-BACE1 Signaling Pathway in Aluminum-Induced Neurotoxicity in PC12 Cells.ACS omega · 2025Article
- A novel isoquinoline mitophagy inducer ameliorates paclitaxel-induced peripheral neuropathy in Drosophila and mouse models.Scientific reports · 2025Article
- Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances.Signal transduction and targeted therapy · 2025Review
- FoxG1/BNIP3 axis promotes mitophagy and blunts cisplatin resistance in osteosarcoma.Cancer science · 2024Article
- Parkin-mediated mitophagy is a potential treatment for oxaliplatin-induced peripheral neuropathy.American journal of physiology. Cell physiology · 2024Article
- Review
- Low-intensity low-frequency pulsed ultrasound ameliorates sciatic nerve dysfunction in a rat model of cisplatin-induced peripheral neuropathy.Scientific reports · 2022Article
- Effect of PINK1 and Parkin gene silencing on sodium arsenite-induced mitophagy in normal rat liver cells (BRL-3A).Toxicology research · 2022Article
- Mini-Review: Mitochondrial dysfunction and chemotherapy-induced neuropathic pain.Neuroscience letters · 2021Review
- Mitophagy Impairment Aggravates Cisplatin-Induced Ototoxicity.BioMed research international · 2021Article
- Review
- Targeting Oxidative Stress, Autophagy, and Apoptosis by Quercetin to Ameliorate Cisplatin-induced Peripheral Neuropathy in Rats.Journal of microscopy and ultrastructureArticle
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND The pathogenesis of chemotherapy-induced neuropathy, a dose-dependent adverse effect of cisplatin, involves mitochondrial dysfunction. PTEN-induced putative kinase 1 (PINK1)/Parkin-mediated mitophagy removes damaged mitochondria under various pathological conditions. The objective of this study was to determine mitophagy status and its effects on mitochondrial function and neuronal cell damage after cisplatin treatment using an in vitro model of cisplatin-induced neurotoxicity. MATERIAL AND METHODS PC12 cells were transfected with Parkin or Parkin siRNA using lentiviral particles and Lipofectamine 3000™, respectively, and then were exposed to 10 μM cisplatin. The expression of autophagic proteins was measured by Western blot analysis. Mitophagy in PC12 cells was detected by confocal microscopy analysis of mitochondria-lysosomes colocalization and autophagic flux. The effects of PINK1/Parkin-mediated mitophagy on cisplatin-induced neurotoxicity were assessed via mitochondrial function, neuritic length, nuclear diameter, and apoptosis. RESULTS Cisplatin activated PINK1/Parkin-mediated mitophagy in PC12 cells. Autophagic flux analysis revealed that cisplatin inhibits the late stage of the autophagic process. The knockdown of Parkin suppressed cisplatin-induced mitophagy, aggravating cisplatin-induced depolarization of mitochondria, cellular ATP deficits, reactive oxygen species outburst, neuritic shortening, nuclear diameter reduction, and apoptosis, while Parkin overexpression enhanced mitophagy and reversed these effects. CONCLUSIONS PINK1/Parkin-regulated mitophagy can protect against cisplatin-related neurotoxicity, suggesting therapeutic enhancement of mitophagy as a potential intervention for cisplatin-induced peripheral neuropathies. The interference of cisplatin with autophagosome-lysosome fusion may be partly responsible for cisplatin-induced neurotoxicity.
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