ArticleScience advances2020
Intracellular delivery of Parkin rescues neurons from accumulation of damaged mitochondria and pathological α-synuclein.
Article in Science advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 69 citations in OpenAlex.
- Mapping the causal chain from genetic risk variants to lipid dysmetabolism in Parkinson's disease.Brain : a journal of neurology · 2026Article
- In vitro and in vivo rescue of dopaminergic neurons in Parkinson's disease models after Parkin gene therapy.Gene therapy · 2026Article
- HUWE1 regulates mitophagy to protect dopaminergic neurons from 6-OHDA- and MPP⁺-induced neurotoxicity.Cell biology and toxicology · 2026Article
- Autophagy and mitophagy at the synapse and beyond: implications for learning, memory and neurological disorders.Autophagy · 2026Review
- Parkin protects against traumatic brain injury through regulating mitochondrial quality control.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Cardiolipin and mitochondrial membrane integrity in neurodegeneration: insights from α-synuclein-driven Parkinson's disease.Acta neuropathologica communications · 2025Review
- Activation of endogenous PRKN by structural derepression is linked to increased turnover of the E3 ubiquitin ligase.Autophagy · 2025Article
- Regulation of mitochondrial dynamics and function by melatonin type 1 receptor in parkinson's disease.Cellular and molecular life sciences : CMLS · 2025Article
- Unlocking Parkinson's disease: the role of microRNAs in regulation, diagnosis, and therapy.Apoptosis : an international journal on programmed cell death · 2025Review
- LRRK2-mediated mitochondrial dysfunction in Parkinson's disease.The Biochemical journal · 2025Review
- TFE3-mediated neuroprotection: Clearance of aggregated α-synuclein and accumulated mitochondria in the AAV-α-synuclein model of Parkinson's disease.Genes & diseases · 2025Article
- Review
- Interplay between α-synuclein and parkin genes: Insights of Parkinson's disease.Molecular biology reports · 2024Review
- Cell-permeable bone morphogenetic protein 2 facilitates bone regeneration by promoting osteogenesis.Materials today. Bio · 2024Article
- Intracellular delivery of Parkin-RING0-based fragments corrects Parkin-induced mitochondrial dysfunction through interaction with SLP-2.Journal of translational medicine · 2024Article
- Intracellular delivery of nuclear localization sequence peptide mitigates COVID-19 by inhibiting nuclear transport of inflammation-associated transcription factors.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Emerging perspectives on precision therapy for Parkinson's disease: multidimensional evidence leading to a new breakthrough in personalized medicine.Frontiers in aging neuroscience · 2024Review
- Liquid-liquid phase separation and conformational strains ofFrontiers in molecular neuroscience · 2024Review
- Nanomotor-based HBioactive materials · 2024Article
- Linking Heat Shock Protein 70 and Parkin in Parkinson's Disease.Molecular neurobiology · 2023Review
Corrections and comments
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Authors and funding
19 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by mitochondrial dysfunction, Lewy body formation, and loss of dopaminergic neurons. Parkin, an E3 ubiquitin ligase, is thought to inhibit PD progression by removing damaged mitochondria and suppressing the accumulation of α-synuclein and other protein aggregates. The present study describes a protein-based therapy for PD enabled by the development of a cell-permeable Parkin protein (iCP-Parkin) with enhanced solubility and optimized intracellular delivery. iCP-Parkin recovered damaged mitochondria by promoting mitophagy and mitochondrial biogenesis and suppressed toxic accumulations of α-synuclein in cells and animals. Last, iCP-Parkin prevented and reversed declines in tyrosine hydroxylase and dopamine expression concomitant with improved motor function induced by mitochondrial poisons or enforced α-synuclein expression. These results point to common, therapeutically tractable features in PD pathophysiology, and suggest that motor deficits in PD may be reversed, thus providing opportunities for therapeutic intervention after the onset of motor symptoms.
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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.