ReviewAntioxidants (Basel, Switzerland)2020
Mitochondrial Dysfunction, Oxidative Stress, and Neuroinflammation: Intertwined Roads to Neurodegeneration.
Review in Antioxidants (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 246 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
246 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Exploring the mechanisms and therapeutic role of γ-oryzanol in neuropathic pain: a systematic review.Inflammopharmacology · 2026Pooled it
- Nigral biochemical and structural alterations following subacute exposure to MPTP in mice.Toxicology reports · 2026Article
- Unraveling the role of FGF21 in epilepsy disease: mechanistic insights and therapeutic Potential.Metabolic brain disease · 2026Review
- Review
- Role of voltage-dependent anion channel 1 in neurodegeneration: Mechanisms, implications, and therapeutic potential.Neural regeneration research · 2026Article
- Montelukast Ameliorates Antimony-Induced Neurotoxicity Accompanied by Alterations in Oxidative Stress, Neuroinflammation, and Mitochondrial Function.Biological trace element research · 2026Article
- Pathogenesis-Driven Drug Repurposing with a Self-Nanoemulsifying Delivery System for Parkinson's Disease.Pharmaceuticals (Basel, Switzerland) · 2026Review
- The central role of mitochondrial dysfunction in neurodegeneration: implications for therapy.Molecular and cellular biochemistry · 2026Review
- Review
- Integrated biomarkers of oxidative stress NLRP3 inflammasome and kynurenine pathway reflect disease severity and diagnostic discrimination in depression.Scientific reports · 2026Article
- Mitochondrial Genetic Diseases and Ophthalmic Manifestations: Molecular Pathophysiology, Genetics, and Clinical Management.International journal of molecular sciences · 2026Review
- Review
- Comparative Study of Young and MaturePlants (Basel, Switzerland) · 2026Article
- Role Shift of Glial Cells from Physiology to Pathology in Alzheimer's Disease: The Regulatory Impact of Exercise.Neuroscience bulletin · 2026Review
- Mitochondrial Dysfunction in Circulating Blood Cells and Biological Aging: A Review of Mechanisms and Evidence.Biomolecules · 2026Review
- Suanzao Ren Decoction Alleviates Anxiety-Like Behavior and Cognitive Dysfunction in Chronic Unpredictable Stress Rats by Modulating Oxidative Stress and Autophagy.Brain and behavior · 2026Article
- iPSC-Derived 3D Brain Organoids as Next-generation Platforms to Study Viral and Toxicant-associated Neurodegeneration.Stem cell reviews and reports · 2026Review
- Endovascular stem cell therapy reconfigures post-stroke ER dynamics via GRP78/Atlastin/CHOP axis.Molecular brain · 2026Article
- A Age Related Vascular Senescence: Mystery of Blood-brain Barrier Dysfunction in Neurodegeneration.Molecular neurobiology · 2026Review
- Designed Liquid Crystalline Nanoassemblies From Clinically Validated Polyunsaturated Lipids for Combined Antioxidant, Anti-Apoptotic, and Neurotrophic Treatments.Advanced healthcare materials · 2026Article
186 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.
Funding
Abstract
Oxidative stress develops as a response to injury and reflects a breach in the cell's antioxidant capacity. Therefore, the fine-tuning of reactive oxygen species (ROS) generation is crucial for preserving cell's homeostasis. Mitochondria are a major source and an immediate target of ROS. Under different stimuli, including oxidative stress and impaired quality control, mitochondrial constituents (e.g., mitochondrial DNA, mtDNA) are displaced toward intra- or extracellular compartments. However, the mechanisms responsible for mtDNA unloading remain largely unclear. While shuttling freely within the cell, mtDNA can be delivered into the extracellular compartment via either extrusion of entire nucleoids or the generation and release of extracellular vesicles. Once discarded, mtDNA may act as a damage-associated molecular pattern (DAMP) and trigger an innate immune inflammatory response by binding to danger-signal receptors. Neuroinflammation is associated with a large array of neurological disorders for which mitochondrial DAMPs could represent a common thread supporting disease progression. The exploration of non-canonical pathways involved in mitochondrial quality control and neurodegeneration may unveil novel targets for the development of therapeutic agents. Here, we discuss these processes in the setting of two common neurodegenerative diseases (Alzheimer's and Parkinson's disease) and Down syndrome, the most frequent progeroid syndrome.
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What OpenQuestion holds
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.