ArticleHuman molecular genetics2017
Sirt3 protects dopaminergic neurons from mitochondrial oxidative stress.
Article in Human molecular genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 123 citations in OpenAlex.
- PARK7/HSPB1-Mediated Neuroprotective Effects of SHED in an In vitro Parkinson's Disease Model.Neurochemical research · 2026Article
- Review
- Targeted metabolomics to assess positive effects of empagliflozin in a Parkinson's disease model: focused on the kynurenine pathway and oxidative stress.Scientific reports · 2026Article
- Histone modification dynamics in brain aging: unlocking therapeutic potential.Cell death & disease · 2026Review
- When R-Loops Go Awry: Genome Instability and Neurological Diseases.The European journal of neuroscience · 2026Review
- Hydrogen sulfide attenuates oxidative stress-induced cellular senescence via the Sirt3/SOD2 signaling pathway in chronic obstructive pulmonary disease.Chinese medical journal · 2026Article
- Comprehensive Proteomic Profiling Reveals Dysregulation of Angiogenesis and Inflammatory Pathways in the Brains of SIRT3 Knockout Mice.Brain sciences · 2026Article
- Role of SIRT3 in digestive system diseases and therapeutic prospects (Review).International journal of molecular medicine · 2026Review
- Mechanistic Links Between the Gut Microbiome and Longevity Therapeutics.Biomedicines · 2026Review
- Melatonin as a Guardian of Mitochondria: Mechanisms and Therapeutic Potential in Neurodegenerative Diseases.Biology · 2026Review
- Therapeutic mechanistic framework of mesenchymal stem cell-derived extracellular vesicles in neurodegenerative diseases.Extracellular vesicles and circulating nucleic acids · 2026Review
- Chronic stress-induced LC-NE dysfunction: cellular and axonal mechanisms underlying impaired neuromodulation.Frontiers in neuroscience · 2026Review
- Mitochondrial sirtuins, key regulators of aging.Life medicine · 2025Review
- Manganese Superoxide Dismutase: Structure, Function, and Implications in Human Disease.Antioxidants (Basel, Switzerland) · 2025Review
- Genetically encoded biosensors of metabolic function for the study of neurodegeneration, a review and perspective.Neurophotonics · 2025Review
- SIRT3-Mediated Deacetylation of DRP1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Redox modulatory role of DJ-1 in Parkinson's disease.Biogerontology · 2025Review
- Oxidative stress and dysregulated long noncoding RNAs in the pathogenesis of Parkinson's disease.Biological research · 2025Review
- The mechanism and therapeutic potential of SIRT3 in central nervous system diseases: a review.Frontiers in pharmacology · 2025Review
- Multi-omics analysis reveals the genetic aging landscape of Parkinson's disease.Scientific reports · 2024Article
5 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
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Age-dependent elevation in mitochondrial oxidative stress is widely posited to be a major factor underlying the loss of substantia nigra pars compacta (SNc) dopaminergic neurons in Parkinson's disease (PD). However, mechanistic links between aging and oxidative stress are not well understood. Sirtuin-3 (Sirt3) is a mitochondrial deacetylase that could mediate this connection. Indeed, genetic deletion of Sirt3 increased oxidative stress and decreased the membrane potential of mitochondria in SNc dopaminergic neurons. This change was attributable to increased acetylation and decreased activity of manganese superoxide dismutase (MnSOD). Site directed mutagenesis of lysine 68 to glutamine (K68Q), mimicking acetylation, decreased MnSOD activity in SNc dopaminergic neurons, whereas mutagenesis of lysine 68 to arginine (K68R), mimicking deacetylation, increased activity. Introduction of K68R MnSOD rescued mitochondrial redox status and membrane potential of SNc dopaminergic neurons from Sirt3 knockouts. Moreover, deletion of DJ-1, which helps orchestrate nuclear oxidant defenses and Sirt3 in mice led to a clear age-related loss of SNc dopaminergic neurons. Lastly, K68 acetylation of MnSOD was significantly increased in the SNc of PD patients. Taken together, our studies suggest that an age-related decline in Sirt3 protective function is a major factor underlying increasing mitochondrial oxidative stress and loss of SNc dopaminergic neurons in PD.
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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.