ArticleDisease models & mechanisms2023
Increased cysteine metabolism in PINK1 models of Parkinson's disease.
Article in Disease models & mechanisms, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 34 citations in OpenAlex.
- Review
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- Exploring the neuroprotective benefits of phytochemicals extracted from indigenous edible fruits in Bangladesh.Animal models and experimental medicine · 2025Review
- A crazy trio in Parkinson's disease: metabolism alteration, α-synuclein aggregation, and oxidative stress.Molecular and cellular biochemistry · 2025Review
- Constraint-based modeling of bioenergetic differences between synaptic and non-synaptic components of dopaminergic neurons in Parkinson's disease.Frontiers in computational neuroscience · 2025Article
- Alzheimer's Disease Pathology and Assistive Nanotheranostic Approaches for Its Therapeutic Interventions.International journal of molecular sciences · 2024Review
- Multi-omics integration of scRNA-seq time series data predicts new intervention points for Parkinson's disease.Scientific reports · 2024Article
- Synergistic modelling of human disease.Disease models & mechanisms · 2024Article
- Recent Progress in the Rational Design of Biothiol-Responsive Fluorescent Probes.Molecules (Basel, Switzerland) · 2023Review
- Blocking dPerk in the intestine suppresses neurodegeneration in a Drosophila model of Parkinson's disease.Cell death & disease · 2023Article
- Uncovering novel therapeutic targets in glucose, nucleotides and lipids metabolism during cancer and neurological diseases.International journal of immunopathology and pharmacologyReview
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Parkinson's disease (PD), an age-dependent neurodegenerative disease, is characterised by the selective loss of dopaminergic neurons in the substantia nigra (SN). Mitochondrial dysfunction is a hallmark of PD, and mutations in PINK1, a gene necessary for mitochondrial fitness, cause PD. Drosophila melanogaster flies with pink1 mutations exhibit mitochondrial defects and dopaminergic cell loss and are used as a PD model. To gain an integrated view of the cellular changes caused by defects in the PINK1 pathway of mitochondrial quality control, we combined metabolomics and transcriptomics analysis in pink1-mutant flies with human induced pluripotent stem cell (iPSC)-derived neural precursor cells (NPCs) with a PINK1 mutation. We observed alterations in cysteine metabolism in both the fly and human PD models. Mitochondrial dysfunction in the NPCs resulted in changes in several metabolites that are linked to cysteine synthesis and increased glutathione levels. We conclude that alterations in cysteine metabolism may compensate for increased oxidative stress in PD, revealing a unifying mechanism of early-stage PD pathology that may be targeted for drug development. This article has an associated First Person interview with the first author of the paper.
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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.