ArticleCNS neuroscience & therapeutics2023
Hypoxic stress accelerates the propagation of pathological alpha-synuclein and degeneration of dopaminergic neurons.
Article in CNS neuroscience & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Chronic intermittent hypoxia increases Parkinson's disease susceptibility via PPARα-mediated lipid droplet-mitochondrial dysfunction.Theranostics · 2026Article
- Exploring the role of HIF-1α in pathogenesis of parkinson's disease and its potential as a therapeutic target.Molecular biology reports · 2025Review
- Unraveling the Mystery of Hemoglobin in Hypoxia-Accelerated Neurodegenerative Diseases.Biomolecules · 2025Review
- Exploring α-Syn's Functions Through Ablation Models: Physiological and Pathological Implications.Cellular and molecular neurobiology · 2025Review
- Big data for neuroscience in the context of predictive, preventive, and personalized medicine.The EPMA journal · 2025Review
- Bridging the gap: investigating the role of phosphorylation at the serine 129 site of α-synuclein in VAPB-PTPIP51 interactions.Acta neuropathologica communications · 2025Article
- Alpha synuclein and inflammaging.Heliyon · 2025Review
- Spiral volumetric optoacoustic tomography of reduced oxygen saturation in the spinal cord of M83 mouse model of Parkinson's disease.European journal of nuclear medicine and molecular imaging · 2025Article
- New Aspects Regarding the Fluorescence Spectra of Melanin and Neuromelanin in Pigmented Human Tissue Concerning Hypoxia.International journal of molecular sciences · 2024Article
- The Role of Oxygen Homeostasis and the HIF-1 Factor in the Development of Neurodegeneration.International journal of molecular sciences · 2024Review
- Hypoxic stress accelerates the propagation of pathological alpha-synuclein and degeneration of dopaminergic neurons.CNS neuroscience & therapeutics · 2023Article
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsThe etiology of Parkinson's disease (PD) is complex and the mechanism is unclear. It has become a top priority to find common factors that induce and affect PD pathology. We explored the key role of hypoxia in promoting the pathological propagation of α-synuclein (α-syn) and the progression of PD.
methodsWe performed PD modeling by conducting intracranial stereotaxic surgery in the unilateral striatum of mice. We then measured protein aggregation in vitro. The rotarod and pole tests were employed next to measure the damage of the phenotype. Pathological deposition and autophagy were also observed by immunofluorescence staining and protein levels measured by western blotting.
resultsWe demonstrated that short-term hypoxia activated phosphorylated (p)-α-syn in mice. We confirmed that p-α-syn was more readily formed aggregates than α-syn in vitro. Furthermore, we found that hypoxia promoted the activation and propagation of endogenous α-syn, contributing to the earlier degeneration of dopaminergic neurons in the substantia nigra and the deposition of p-α-syn in our animal model. Finally, autophagy inhibition contributed to the above pathologies.
conclusionHypoxia was shown to accelerate the pathological progression and damage phenotype in PD model mice. The results provided a promising research target for determining common interventions for PD in the future.
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