ReviewFrontiers in molecular biosciences2022
Mitochondrial ATP Synthase is a Target of Oxidative Stress in Neurodegenerative Diseases.
Review in Frontiers in molecular biosciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 56 citations in OpenAlex.
- The Interplay of Metabolic Dysfunction, Neuroinflammation, and Mitochondrial Dysfunction in Balance Impairment: Insights from Type 2 Diabetes Mellitus and Alzheimer's Disease.Molecular neurobiology · 2026Review
- Distinct single-nucleus RNA-seq changes among non-neuronal cells in ADNC, LATE-NC, and mixed pathologies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- LPAR4 mediates resistance to interferon-induced stress in soft tissue sarcoma.Science advances · 2026Article
- Article
- Nucleotide Exchange Mechanism Involving Angle-Dependent Rate Constants Extracted from F1-ATPase Single-Molecule Rotation Trajectories.The journal of physical chemistry. B · 2026Article
- Soluble guanylate cyclase deficiency drives retinal ganglion cell neurodegeneration with age in female mice through disrupted oxidative metabolism.Scientific reports · 2026Article
- Systematic Characterization of LUHMES Cell-Based Parkinson's Disease Models Reveals Potential Novel Drug Targets.Molecular neurobiology · 2025Article
- Parkinson's associated protein DJ-1 regulates intercellular communication via extracellular vesicles in oxidative stress.Cell death discovery · 2025Article
- The Redox Revolution in Brain Medicine: Targeting Oxidative Stress with AI, Multi-Omics and Mitochondrial Therapies for the Precision Eradication of Neurodegeneration.International journal of molecular sciences · 2025Review
- ATP Synthase Abundance in Neuronal Extracellular Vesicles Reflects Changes in the Mitochondria of Parent Neurons.Journal of extracellular vesicles · 2025Article
- SLC5A3 depletion promotes apoptosis by inducing mitochondrial dysfunction and mitophagy in gemcitabine-resistant pancreatic cancer cells.Cell death & disease · 2025Article
- Oxidative stress and inflammation in the pathogenesis of neurological disorders: Mechanisms and implications.Acta pharmaceutica Sinica. B · 2025Review
- Prospects for nasal delivery of a pharmacologic agent for neuroprotective experimental therapy after prenatal hypoxia.Frontiers in systems neuroscience · 2025Article
- The neurotoxicity of iodoacetic acid, a byproduct of drinking water disinfection.Frontiers in toxicology · 2025Review
- Activation of the Keap1/Nrf2/HO-1 Pathway by "Tianyu" Pairing: Implications for Inflammation and Oxidative Stress in Rheumatoid Arthritis.Endocrine, metabolic & immune disorders drug targets · 2025Article
- The Role of Iron Metabolism in Sepsis-associated Encephalopathy: a Potential Target.Molecular neurobiology · 2024Review
- Cultured Rat Hippocampal Neurons Exposed to the Mitochondrial Uncoupler Carbonyl Cyanide Chlorophenylhydrazone Undergo a Rapid, Presenilin-Dependent Change in Neuronal Properties.International journal of molecular sciences · 2024Article
- Pyrroloquinoline quinone drives ATP synthesis in vitro and in vivo and provides retinal ganglion cell neuroprotection.Acta neuropathologica communications · 2023Article
- Overcoming mitochondrial dysfunction in neurodegenerative diseases.Neural regeneration research · 2023Article
- Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mitochondrial ATP synthase is responsible for the production of cellular ATP, and it does so by harnessing the membrane potential of the mitochondria that is produced by the sequential oxidation of select cellular metabolites. Since the structural features of ATP synthase were first resolved nearly three decades ago, significant progress has been made in understanding its role in health and disease. Mitochondrial dysfunction is common to neurodegeneration, with elevated oxidative stress a hallmark of this dysfunction. The patterns of this oxidative stress, including molecular targets and the form of oxidative modification, can vary widely. In this mini review we discuss the oxidative modifications of ATP synthase that have been observed in Alzheimer's disease, Parkinson's disease, and Huntington's disease. Oxidative modifications of ATP synthase in Alzheimer's disease are well-documented, and there is a growing body of knowledge on the subject in Parkinson's disease. The consideration of ATP synthase as a pharmacological target in a variety of diseases underlines the importance of understanding these modifications, both as a potential target, and also as inhibitors of any pharmacological intervention.
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