ArticleHuman molecular genetics2018
Superoxide dismutating molecules rescue the toxic effects of PINK1 and parkin loss.
Article in Human molecular genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Role of Oxidative Stress in Human Neurodegenerative Pathologies: Lessons from theCurrent topics in medicinal chemistry · 2026Review
- High-saturated-fat diet drives female-biased neurodegeneration inFrontiers in aging neuroscience · 2026Article
- Inhibition of K63 ubiquitination by G-Protein pathway suppressor 2 (GPS2) regulates mitochondria-associated translation.Pharmacological research · 2024Article
- Elevated Level of PINK1/Parkin-Mediated Mitophagy Pathway Involved to the Inhibited Activity of Mitochondrial Superoxide Dismutase in Rat Brains and Primary Hippocampal Neurons Exposed to High Level of Fluoride.Biological trace element research · 2024Article
- Evidence for Oxidative Pathways in the Pathogenesis of PD: Are Antioxidants Candidate Drugs to Ameliorate Disease Progression?International journal of molecular sciences · 2022Review
- Maintenance of mitochondrial integrity in midbrain dopaminergic neurons governed by a conserved developmental transcription factor.Nature communications · 2022Article
- An assessment of the rescue action of resveratrol in parkin loss of function-induced oxidative stress in Drosophila melanogaster.Scientific reports · 2022Article
- Metabolic Alterations in aCells · 2022Article
- "Metal elements and pesticides as risk factors for Parkinson's disease - A review".Toxicology reports · 2021Review
- Role of Commensal Microbes in the γ-Ray Irradiation-Induced Physiological Changes inMicroorganisms · 2020Article
- Article
- The STING pathway does not contribute to behavioural or mitochondrial phenotypes in Drosophila Pink1/parkin or mtDNA mutator models.Scientific reports · 2020Article
- Antioxidant Therapy in Parkinson's Disease: Insights fromAntioxidants (Basel, Switzerland) · 2020Review
- Molecular Mechanisms Underlying Reciprocal Interactions Between Sleep Disorders and Parkinson's Disease.Frontiers in neuroscience · 2020Review
- Oxidative Stress in Parkinson's Disease: Potential Benefits of Antioxidant Supplementation.Oxidative medicine and cellular longevity · 2020Review
- Oxidative stress in the aging substantia nigra and the etiology of Parkinson's disease.Aging cell · 2019Review
- Superoxide Dismutases SOD1 and SOD2 Rescue the Toxic Effect of Dopamine-Derived Products in Human SH-SY5Y Neuroblastoma Cells.Neurotoxicity research · 2019Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Reactive oxygen species exert important functions in regulating several cellular signalling pathways. However, an excessive accumulation of reactive oxygen species can perturb the redox homeostasis leading to oxidative stress, a condition which has been associated to many neurodegenerative disorders. Accordingly, alterations in the redox state of cells and mitochondrial homeostasis are established hallmarks in both familial and sporadic Parkinson's disease cases. PINK1 and Parkin are two genes which account for a large fraction of autosomal recessive early-onset forms of Parkinson's disease and are now firmly associated to both mitochondria and redox homeostasis. In this study we explored the hypothesis that superoxide anions participate in the generation of the Parkin and PINK1 associated phenotypic effect by testing the capacity of endogenous and exogenous superoxide dismutating molecules to rescue the toxic effects induced by loss of PINK1 or Parkin, in both cellular and fly models. Our results demonstrate the positive effect of an increased level of superoxide dismutase proteins on the pathological phenotypes, both in vitro and in vivo. A more pronounced effectiveness for mitochondrial SOD2 activity points to the superoxide radicals generated in the mitochondrial matrix as the prime suspect in the definition of the observed phenotypes. Moreover, we also demonstrate the efficacy of a SOD-mimetic compound, M40403, to partially ameliorate PINK1/Parkin phenotypes in vitro and in vivo. These results support the further exploration of SOD-mimetic compounds as a therapeutic strategy against Parkinson's disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.