ArticleCommunications biology2023
ACO2 deficiency increases vulnerability to Parkinson's disease via dysregulating mitochondrial function and histone acetylation-mediated transcription of autophagy genes.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- Unraveling the molecular landscape and therapeutic strategies for acute kidney injury: insights from transcriptomics, network pharmacology, virtual screening, and in vitro experiments.Molecular diversity · 2026Article
- Citric Acid Cycle Genes and Nutrigenetics.International journal of molecular sciences · 2026Review
- Regulation of mitochondrial iron homeostasis in tumor cells.Molecular medicine (Cambridge, Mass.) · 2026Review
- Precision targeting of FDX1-mediated cuproptosis by a ROS-responsive hydrogel for myocardial ischemia-reperfusion injury treatment.Theranostics · 2026Article
- N-lactoyl amino acids are potential biomarkers for insulin resistance and diabetic complications.Diabetes, obesity & metabolism · 2025Article
- Infantile Cerebellar-Retinal Degeneration Associated With Novel ACO2 Variants: Clinical Features and Insights From a Drosophila Model.Clinical genetics · 2025Article
- Mitochondrial dysfunction-mediated metabolic remodeling of TCA cycle promotes Parkinson's disease through inhibition of H3K4me3 demethylation.Cell death discovery · 2025Article
- Metabolic Dysregulation in Parkinson's Disease: Non-Oxidative Phosphorylation and Its Role in Brain Energy Metabolism.Aging and disease · 2025Review
- Analysis and identification of mitochondria-related genes associated with age-related hearing loss.BMC genomics · 2025Article
- N88S seipin-related seipinopathy is a lipidopathy associated with loss of iron homeostasis.Cell communication and signaling : CCS · 2025Article
- Including genetic susceptibility towards Parkinson's disease in NAM-based hazard and risk assessment of pesticides: a semi-systematic review.NAM journal · 2025Review
- Proteomic landscape of porcine induced neural stem cell reprogramming and differentiation.PeerJ · 2025Article
- Platinum(IV) anticancer therapies and cathepsin B: innovative strategies for overcoming resistance in glioblastoma cells.Frontiers in cell and developmental biology · 2025Article
- In situ stoichiometry amounts of p62 and poly-ubiquitin exceed the increase of alpha-synuclein during degeneration of catecholamine cells induced by autophagy inhibition in vitro.Journal of neural transmission (Vienna, Austria : 1996) · 2024Article
- Binding of α-synuclein to ACO2 promotes progressive mitochondrial dysfunction in Parkinson's disease models.Redox biology · 2024Article
- Mitochondrial Aconitase and Its Contribution to the Pathogenesis of Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Mitochondrial DNA Instability Supersedes Parkin Mutations in Driving Mitochondrial Proteomic Alterations and Functional Deficits in Polg Mutator Mice.International journal of molecular sciences · 2024Article
- Is There a Place for Lewy Bodies before and beyond Alpha-Synuclein Accumulation? Provocative Issues in Need of Solid Explanations.International journal of molecular sciences · 2024Review
- Mitochondrial stress-induced H4K12 hyperacetylation dysregulates transcription in Parkinson's disease.Frontiers in cellular neuroscience · 2024Article
- Transcriptome analyses reveal molecular mechanisms of novel compound heterozygousFrontiers in cellular neuroscience · 2024Article
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Authors and funding
9 authors at 1 institution in 1 country.
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Abstract
Parkinson's disease (PD) is characterized by α-synuclein aggregation in dopaminergic (DA) neurons, which are sensitive to oxidative stress. Mitochondria aconitase 2 (ACO2) is an essential enzyme in the tricarboxylic acid cycle that orchestrates mitochondrial and autophagic functions to energy metabolism. Though widely linked to diseases, its relation to PD has not been fully clarified. Here we revealed that the peripheral ACO2 activity was significantly decreased in PD patients and associated with their onset age and disease durations. The knock-in mouse and Drosophila models with the A252T variant displayed aggravated motor deficits and DA neuron degeneration after 6-OHDA and rotenone-induction, and the ACO2 knockdown or blockade cells showed features of mitochondrial and autophagic dysfunction. Moreover, the transcription of autophagy-related genes LC3 and Atg5 was significantly downregulated via inhibited histone acetylation at the H3K9 and H4K5 sites. These data provided multi-dimensional evidences supporting the essential roles of ACO2, and as a potential early biomarker to be used in clinical trials for assessing the effects of antioxidants in PD. Moreover, ameliorating energy metabolism by targeting ACO2 could be considered as a potential therapeutic strategy for PD and other neurodegenerative disorders.
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