ArticleGlia2013
PINK1 deficiency attenuates astrocyte proliferation through mitochondrial dysfunction, reduced AKT and increased p38 MAPK activation, and downregulation of EGFR.
Article in Glia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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.
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.
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Who cites it
53 citing papers in PubMed, 89 citations in OpenAlex.
- PINK1 loss in astrocytes triggers inflammatory dysfunction and neuronal death.bioRxiv : the preprint server for biology · 2026Article
- LRP10 and α-synuclein transmission in Lewy body diseases.Cellular and molecular life sciences : CMLS · 2024Article
- Role of Astrogliosis in the Pathogenesis of Parkinson's Disease: Insights into Astrocytic Nrf2 Pathway as a Potential Therapeutic Target.CNS & neurological disorders drug targets · 2024Review
- Role of Astrocytes in Parkinson's Disease Associated with Genetic Mutations and Neurotoxicants.Cells · 2023Review
- The Synucleins and the Astrocyte.Biology · 2023Review
- Astrocyte contribution to dysfunction, risk and progression in neurodegenerative disorders.Nature reviews. Neuroscience · 2023Review
- The Fault in Our Astrocytes - cause or casualties of proteinopathies of ALS/FTD and other neurodegenerative diseases?Frontiers in molecular medicine · 2023Review
- Multifaceted roles of mitochondria in wound healing and chronic wound pathogenesis.Frontiers in cell and developmental biology · 2023Review
- Brain Energy Metabolism: Astrocytes in Neurodegenerative Diseases.CNS neuroscience & therapeutics · 2023Review
- Age-Associated Glia Remodeling and Mitochondrial Dysfunction in Neurodegeneration: Antioxidant Supplementation as a Possible Intervention.Nutrients · 2022Review
- Therapeutic application of quercetin in aging-related diseases: SIRT1 as a potential mechanism.Frontiers in immunology · 2022Review
- PTEN-Induced Putative Kinase 1 Dysfunction Accelerates Synucleinopathy.Journal of Parkinson's disease · 2022Article
- Astrocyte dysfunction in Parkinson's disease: from the perspectives of transmitted α-synuclein and genetic modulation.Translational neurodegeneration · 2021Review
- Astrocytes, a Promising Opportunity to Control the Progress of Parkinson's Disease.Biomedicines · 2021Review
- The PINK1-Mediated Crosstalk between Neural Cells and the Underlying Link to Parkinson's Disease.Cells · 2021Review
- The ATP Synthase Deficiency in Human Diseases.Life (Basel, Switzerland) · 2021Review
- Depletion of Mitochondrial Components from Extracellular Vesicles Secreted from Astrocytes in a Mouse Model of Fragile X Syndrome.International journal of molecular sciences · 2021Article
- Astrocyte-Neuron Metabolic Crosstalk in Neurodegeneration: A Mitochondrial Perspective.Frontiers in endocrinology · 2021Review
- Review
- PINK1/PARKIN signalling in neurodegeneration and neuroinflammation.Acta neuropathologica communications · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
PINK1 (PTEN induced putative kinase 1), a familial Parkinson's disease (PD)-related gene, is expressed in astrocytes, but little is known about its role in this cell type. Here, we found that astrocytes cultured from PINK1-knockout (KO) mice exhibit defective proliferative responses to epidermal growth factor (EGF) and fetal bovine serum. In PINK1-KO astrocytes, basal and EGF-induced p38 activation (phosphorylation) were increased whereas EGF receptor (EGFR) expression and AKT activation were decreased. p38 inhibition (SB203580) or knockdown with small interfering RNA (siRNA) rescued EGFR expression and AKT activation in PINK1-KO astrocytes. Proliferation defects in PINK1-KO astrocytes appeared to be linked to mitochondrial defects, manifesting as decreased mitochondrial mass and membrane potential, increased intracellular reactive oxygen species level, decreased glucose-uptake capacity, and decreased ATP production. Mitochondrial toxin (oligomycin) and a glucose-uptake inhibitor (phloretin) mimicked the PINK1-deficiency phenotype, decreasing astrocyte proliferation, EGFR expression and AKT activation, and increasing p38 activation. In addition, the proliferation defect in PINK1-KO astrocytes resulted in a delay in the wound healing process. Taken together, these results suggest that PINK1 deficiency causes astrocytes dysfunction, which may contribute to the development of PD due to delayed astrocytes-mediated repair of microenvironment in the brain.
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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.