ArticleNature cell biology2014
Enhancing nucleotide metabolism protects against mitochondrial dysfunction and neurodegeneration in a PINK1 model of Parkinson's disease.
Article in Nature cell biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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Who cites it
85 citing papers in PubMed, 164 citations in OpenAlex.
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- Caspofungin Reshapes the Extracellular Vesicles Metabolome ofJournal of fungi (Basel, Switzerland) · 2026Article
- Insights into PINK1/Parkin function and dysfunction from Drosophila models.The Biochemical journal · 2025Review
- Increased nucleotide metabolism alleviates Alzheimer's disease pathology.Cell death & disease · 2025Article
- In vivo and in silico models of Drosophila for Parkinson's disease.The FEBS journal · 2025Review
- A Drosophila model of prion disease and its metabolic changes in the brain.Animal models and experimental medicine · 2025Article
- Loss of Drosophila ribosomal protein S6 kinase II causes mitochondrial dysfunction and cell death.Disease models & mechanisms · 2025Article
- Review
- Enhancing mitochondrial one-carbon metabolism is neuroprotective in Alzheimer's disease models.Cell death & disease · 2024Article
- Cephalic ganglia transcriptomics of the American cockroach Periplaneta americana (Blattodea: Blattidae).Journal of insect science (Online) · 2024Article
- Mitochondrial One-Carbon Metabolism and Alzheimer's Disease.International journal of molecular sciences · 2024Review
- Article
- Function and Mechanism of Abscisic Acid on Microglia-Induced Neuroinflammation in Parkinson's Disease.International journal of molecular sciences · 2024Review
- Mitochondrial Differentiation during Spermatogenesis: Lessons fromInternational journal of molecular sciences · 2024Review
- A new metabolic model ofLife science alliance · 2023Article
- Modulating p38 MAPK signaling by proteostasis mechanisms supports tissue integrity during growth and aging.Nature communications · 2023Article
- Blocking dPerk in the intestine suppresses neurodegeneration in a Drosophila model of Parkinson's disease.Cell death & disease · 2023Article
- Evaluation of therapeutic effects of tetramethylpyrazine nitrone in Alzheimer's disease mouse model and proteomics analysis.Frontiers in pharmacology · 2023Article
- Increased cysteine metabolism in PINK1 models of Parkinson's disease.Disease models & mechanisms · 2023Article
- Proteomic Profiling Revealed Mitochondrial Dysfunction in Photoreceptor Cells under Hyperglycemia.International journal of molecular sciences · 2022Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
Mutations in PINK1 cause early-onset Parkinson's disease (PD). Studies in Drosophila melanogaster have highlighted mitochondrial dysfunction on loss of Pink1 as a central mechanism of PD pathogenesis. Here we show that global analysis of transcriptional changes in Drosophila pink1 mutants reveals an upregulation of genes involved in nucleotide metabolism, critical for neuronal mitochondrial DNA synthesis. These key transcriptional changes were also detected in brains of PD patients harbouring PINK1 mutations. We demonstrate that genetic enhancement of the nucleotide salvage pathway in neurons of pink1 mutant flies rescues mitochondrial impairment. In addition, pharmacological approaches enhancing nucleotide pools reduce mitochondrial dysfunction caused by Pink1 deficiency. We conclude that loss of Pink1 evokes the activation of a previously unidentified metabolic reprogramming pathway to increase nucleotide pools and promote mitochondrial biogenesis. We propose that targeting strategies enhancing nucleotide synthesis pathways may reverse mitochondrial dysfunction and rescue neurodegeneration in PD and, potentially, other diseases linked to mitochondrial impairment.
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