ArticleThe Journal of biological chemistry2015
Nitric oxide induction of Parkin translocation in PTEN-induced putative kinase 1 (PINK1) deficiency: functional role of neuronal nitric oxide synthase during mitophagy.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Superoxide signals for the mitophagy of dysfunctional mitochondria to maintain quality control.Redox biology · 2026Review
- Integrated transcriptomics and metabolomics studies reveal the therapeutic effects of Astragalus polysaccharides on cancer cachexia muscle atrophy.Scientific reports · 2025Article
- Parkin Precipitates on Mitochondria via Aggregation and Autoubiquitination.International journal of molecular sciences · 2023Article
- Autophagy: A Key Regulator of Homeostasis and Disease: An Overview of Molecular Mechanisms and Modulators.Cells · 2022Review
- Article
- Protein S-nitrosylation and oxidation contribute to protein misfolding in neurodegeneration.Free radical biology & medicine · 2021Review
- Mitophagy in Human Diseases.International journal of molecular sciences · 2021Review
- Multitasking guardian of mitochondrial quality: Parkin function and Parkinson's disease.Translational neurodegeneration · 2021Review
- Mechanisms of TLR4-Mediated Autophagy and Nitroxidative Stress.Frontiers in cellular and infection microbiology · 2021Review
- Nitric Oxide-Dependent Protein Post-Translational Modifications Impair Mitochondrial Function and Metabolism to Contribute to Neurodegenerative Diseases.Antioxidants & redox signaling · 2020Review
- Vitamin K2 Can Rescue the Dexamethasone-Induced Downregulation of Osteoblast Autophagy and Mitophagy Thereby Restoring Osteoblast FunctionFrontiers in pharmacology · 2020Article
- Macula Densa SGLT1-NOS1-Tubuloglomerular Feedback Pathway, a New Mechanism for Glomerular Hyperfiltration during Hyperglycemia.Journal of the American Society of Nephrology : JASN · 2019Article
- Multiple pathways for mitophagy: A neurodegenerative conundrum for Parkinson's disease.Neuroscience letters · 2019Review
- Recent Insights into the Mitochondrial Role in Autophagy and Its Regulation by Oxidative Stress.Oxidative medicine and cellular longevity · 2019Review
- Melatonin activates Parkin translocation and rescues the impaired mitophagy activity of diabetic cardiomyopathy through Mst1 inhibition.Journal of cellular and molecular medicine · 2018Article
- The Role of Mitophagy in Innate Immunity.Frontiers in immunology · 2018Review
- S-Nitrosylation of PINK1 Attenuates PINK1/Parkin-Dependent Mitophagy in hiPSC-Based Parkinson's Disease Models.Cell reports · 2017Article
- Inhibition of HIF1α and PDK Induces Cell Death of Glioblastoma Multiforme.Experimental neurobiology · 2017Article
- Article
- NDPK-D (NM23-H4)-mediated externalization of cardiolipin enables elimination of depolarized mitochondria by mitophagy.Cell death and differentiation · 2016Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The failure to trigger mitophagy is implicated in the pathogenesis of familial Parkinson disease that is caused by PINK1 or Parkin mutations. According to the prevailing PINK1-Parkin signaling model, mitophagy is promoted by the mitochondrial translocation of Parkin, an essential PINK1-dependent step that occurs via a previously unknown mechanism. Here we determined that critical concentrations of NO was sufficient to induce the mitochondrial translocation of Parkin even in PINK1 deficiency, with apparent increased interaction of full-length PINK1 accumulated during mitophagy, with neuronal nitric oxide synthase (nNOS). Specifically, optimum levels of NO enabled PINK1-null dopaminergic neuronal cells to regain the mitochondrial translocation of Parkin, which appeared to be significantly suppressed by nNOS-null mutation. Moreover, nNOS-null mutation resulted in the same mitochondrial electron transport chain (ETC) enzyme deficits as PINK1-null mutation. The involvement of mitochondrial nNOS activation in mitophagy was further confirmed by the greatly increased interactions of full-length PINK1 with nNOS, accompanied by mitochondrial accumulation of phospho-nNOS (Ser(1412)) during mitophagy. Of great interest is that the L347P PINK1 mutant failed to bind to nNOS. The loss of nNOS phosphorylation and Parkin accumulation on PINK1-deficient mitochondria could be reversed in a PINK1-dependent manner. Finally, non-toxic levels of NO treatment aided in the recovery of PINK1-null dopaminergic neuronal cells from mitochondrial ETC enzyme deficits. In summary, we demonstrated the full-length PINK1-dependent recruitment of nNOS, its activation in the induction of Parkin translocation, and the feasibility of NO-based pharmacotherapy for defective mitophagy and ETC enzyme deficits in Parkinson disease.
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