ArticleCell death & disease2017
Pink1 interacts with α-synuclein and abrogates α-synuclein-induced neurotoxicity by activating autophagy.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Rethinking 'rare'Journal of Parkinson's disease · 2025Pooled it
- Species-dependent activities of the PINK1-parkin axis.Translational neurodegeneration · 2026Review
- Tissue-specific mutation of pink-1 jointly induces intestinal dysfunction and contributes to dopaminergic neuron degeneration.NPJ Parkinson's disease · 2026Article
- Regional gene expression and brain atrophy in dementia with Lewy bodies: an imaging transcriptomics study.NPJ Parkinson's disease · 2026Article
- Exercise suppresses apoptosis for alleviating Parkinson's disease: effects on pathophysiological molecular pathways.Frontiers in aging neuroscience · 2026Review
- LINC-EPS Protects Against Neurodegeneration by Driving a PGC-1α-Mediated Anti-Ferroptosis Program in Parkinson's Disease.International journal of biological sciences · 2026Article
- Mitochondrial dysfunction in cellular senescence: a bridge to neurodegenerative disease.npj aging · 2025Review
- The Impact of Neurotoxin Proteins Trafficked by Primary Cilia and Extracellular Vesicles in Neurodegenerative Diseases.Biology · 2025Review
- Bridging the gap in Parkinson's disease research: from general pathophysiology to advanced 3d cell culture models.Cell communication and signaling : CCS · 2025Review
- Research on the Application of Mesenchymal Stem Cells for Addressing Mitochondrial Damage in Neurodegenerative Diseases.Cellular and molecular neurobiology · 2025Review
- PINK1 deficiency permits the development of Lewy body dementia with coexisting Aβ pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- A heterozygous variation of PINK1 is potentially associated with essential tremor in a Chinese family.Neurogenetics · 2025Article
- Multifaceted Roles of AFG3L2, a Mitochondrial ATPase in Relation to Neurological Disorders.Molecular neurobiology · 2024Review
- Thioredoxin-1 decreases alpha-synuclein induced by MPTP through promoting autophagy-lysosome pathway.Cell death discovery · 2024Article
- Emerging role of microglia in inter-cellular transmission of α-synuclein in Parkinson's disease.Frontiers in aging neuroscience · 2024Review
- Detection of elevated levels of PINK1 in plasma from patients with idiopathic Parkinson's disease.Frontiers in aging neuroscience · 2024Article
- Towards Understanding Neurodegenerative Diseases: Insights fromInternational journal of molecular sciences · 2023Review
- Thyroarytenoid Oxidative Metabolism and Synaptic Signaling Dysregulation in the Female Pink1-/- Rat.The Laryngoscope · 2023Article
- Involvement of Mitochondria in Parkinson's Disease.International journal of molecular sciences · 2023Review
- Targeting mitophagy for neurological disorders treatment: advances in drugs and non-drug approaches.Naunyn-Schmiedeberg's archives of pharmacology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is one of the most common neurodegenerative diseases, characterized by degeneration of dopaminergic neurons in the substantia nigra. α-synuclein (α-syn) and PTEN-induced putative kinase (PINK)1 are two critical proteins associated with the pathogenesis of PD. α-syn induces mitochondrial deficits and apoptosis, PINK1 was found to alleviate α-syn-induced toxicity, but the mechanistic details remain obscure. Here, we show that PINK1 interacts with α-syn mainly in the cytoplasm, where it initiates autophagy. This interaction was dependent on the kinase activity of PINK1 and was abolished by deletion of the kinase domain or a G309D point mutation, an inactivating mutation in the kinase domain. Interaction between PINK1 and α-syn stimulated the removal of excess α-syn, which prevented mitochondrial deficits and apoptosis. Our findings provide evidence for a novel mechanism underlying the protective effects of PINK1 against α-syn-induced neurodegeneration and highlight a novel therapeutic target for PD treatment.
Indexed as
Identifiers
What OpenQuestion holds
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.