ArticleActa pharmacologica Sinica2024
Cell senescence induced by toxic interaction between α-synuclein and iron precedes nigral dopaminergic neuron loss in a mouse model of Parkinson's disease.
Article in Acta pharmacologica Sinica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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38 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.
- Association between iron deposition and emotional disorder in Parkinson's patients: a systematic review and meta-analysis.BMC neurology · 2026Pooled it
- Mitochondrial transplantation reverses the senescence phenotype of SH-SY5Y cells.Molecular therapy. Advances · 2026Article
- Rethinking Senescence Hallmarks in the Brain: Lessons From Peripheral Tissues and Challenges in Defining Neuronal Senescence.Aging cell · 2026Review
- Ginsenosides: potential therapeutic implications in neurodegenerative diseases by inhibiting ferroptosis.Molecular biology reports · 2026Review
- Epigenetic reprogramming periosteum promotes aging critical segmental bone defect repair via methylation remodeling.Bioactive materials · 2026Article
- Ferritin in ferroptosis: Implications for neurodegenerative diseases (Review).International journal of molecular medicine · 2026Review
- Metal Modulation of Oxytocin Structure, Function, and Receptor Interactions.European journal of inorganic chemistry · 2026Article
- NLRP3 facilitates α-synuclein-induced dopaminergic neuronal senescence in a mouse model of Parkinson's disease through SATB1/DNA damage/p21 signaling pathway.Acta pharmacologica Sinica · 2026Article
- α-synuclein triggers NCOA4-FTH1-mediated ferroptosis of oligodendrocyte in multiple system atrophy.Acta neuropathologica · 2026Article
- Ferroptosis in Parkinson's disease: a review of molecular mechanisms and emerging therapeutic strategies.Frontiers in neuroscience · 2026Review
- Cleaning, Chasing and Calming: Promising Paradigms of Senotherapy in Aging-Related Diseases.International journal of biological sciences · 2026Review
- Parkinson's Disease: The Epidemiology, Risk Factors, Molecular Pathogenesis, Prevention, and Therapy.MedComm · 2025Review
- Innovations in cancer treatment as novel potential and the myth of personalized vaccines, immunotherapy, CRISPR/Cas9, and bacteriotherapy as promising therapeutic strategies.Discover oncology · 2025Review
- Immunosenescence in aging and neurodegenerative diseases: evidence, key hallmarks, and therapeutic implications.Translational neurodegeneration · 2025Review
- HSPA4 restrains transferrin in dopaminergic neurons to attenuate ferroptosis in a Parkinson's disease model.Communications biology · 2025Article
- Investigating the ageing-Parkinson's disease nexus: standardisation of in vitro models and techniques by the PD-AGE network.NPJ Parkinson's disease · 2025Review
- From Bench to Brain: Translating EV and Nanocarrier Research into Parkinson's Disease Therapies.Biology · 2025Review
- DNA Damage Response Regulation Alleviates Neuroinflammation in a Mouse Model of α-Synucleinopathy.Biomolecules · 2025Article
- Role of Cellular Senescence in Parkinson's Disease: Potential for Disease-Modification Through Senotherapy.Biomedicines · 2025Review
- A hypothesis explaining Alzheimer's disease, Parkinson's disease, and dementia with Lewy bodies overlap.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
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9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell senescence has been implicated in the pathology of Parkinson's disease (PD). Both abnormal α-synuclein aggregation and iron deposition are suggested to be the triggers, facilitators, and aggravators during the development of PD. In this study, we investigated the involvement of α-synuclein and iron in the process of cell senescence in a mouse model of PD. In order to overexpress α-syn-A53T in the substantia nigra pars compacta (SNpc), human α-syn-A53T was microinjected into both sides of the SNpc in mice. We found that overexpression of α-syn-A53T for one week induced significant pro-inflammatory senescence-associated secretory phenotype (SASP), increased cell senescence-related proteins (β-gal, p16, p21, H2A.X and γ-H2A.X), mitochondrial dysfunction accompanied by dysregulation of iron-related proteins (L-ferritin, H-ferritin, DMT1, IRP1 and IRP2) in the SNpc. In contrast, significant loss of nigral dopaminergic neurons and motor dysfunction were only observed after overexpression of α-syn-A53T for 4 weeks. In PC12 cells stably overexpressing α-syn-A53T, iron overload (ferric ammonium citrate, FAC, 100 μM) not only increased the level of reactive oxygen species (ROS), p16 and p21, but also exacerbated the processes of oxidative stress and cell senescence signalling induced by α-syn-A53T overexpression. Interestingly, reducing the iron level with deferoxamine (DFO) or knockdown of transferrin receptor 1 (TfR1) significantly improved both the phenotypes and dysregulated proteins of cell senescence induced by α-syn-A53T overexpression. All these evidence highlights the toxic interaction between iron and α-synuclein inducing cell senescence, which precedes nigral dopaminergic neuronal loss in PD. Further investigation on cell senescence may yield new therapeutic agents for the prevention or treatment of PD.
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