ReviewInternational journal of molecular sciences2021
Epigenetic Regulation of Neuroinflammation in Parkinson's Disease.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.
- C/EBPβ as a master regulator of inflammasome signaling in neurodegenerative diseases: mechanisms and therapeutic implications.Frontiers in immunology · 2025Pooled it
- A new paradigm in Parkinson's disease: kidney-origin α-synuclein pathology driven by PKC signaling and aurothioglucose.Inflammopharmacology · 2026Review
- Exercise, Demethylase FTO, Neurological Disorders, and Neuropathic Pain: Potential Molecular Mechanisms.CNS neuroscience & therapeutics · 2026Review
- Silicon quantum dots for neurotheranostic applications in dopamine detection.Journal of nanobiotechnology · 2026Review
- Epigenetic activation of PDLIM7 via H3K27 acetylation mitigates neuroinflammation and neurodegeneration in parkinson's disease models.Journal of bioenergetics and biomembranes · 2026Article
- Unraveling Parkinson's disease: The mystery of mitochondria and the role of aging.Genes & diseases · 2026Review
- TLR4-Mediated Immune Dysfunction Links MASLD and Parkinson's Disease: Insights from an Omics-Based Network Analysis.NeuroSci · 2026Article
- Genome-wide DNA methylation profiling in COVID-19 positive patients reveals alterations in pathways linked to neurological dysfunction.Clinical epigenetics · 2026Article
- Mitochondrial Dynamics-Related Gene Regulation by Epigenetic Suppression of GCN5 Exerts Neuroprotective Effects in Rotenone-Induced Parkinson's Disease Model.Molecular neurobiology · 2026Article
- PM2.5 as a driver of human health disorders: insights from the regulated cell death pathways.Military Medical Research · 2026Review
- Parkinson's disease: genetics and neuroinflammatory insights.Inflammopharmacology · 2025Review
- Microglial immune memory in Parkinson's and Huntington's diseases: epigenetics, triggers, and therapies.Epigenomics · 2025Review
- MicroRNAs Modulating Neuroinflammation in Parkinson's disease.Inflammation · 2025Review
- Associations between inflammation and striatal dopamine D2-receptor availability in aging.Journal of neuroinflammation · 2025Article
- Peripheral-central immune interactions in Parkinson's disease: insights into innate and adaptive immunity.Frontiers in molecular neuroscience · 2025Review
- Druggable Targets for Pelvic Inflammatory Disease: Mendelian Randomization and Experimental Validation.Journal of inflammation research · 2025Article
- Non-coding RNAs as key players in neurodegeneration and brain tumors: Insights into therapeutic strategies.Iranian journal of basic medical sciences · 2025Review
- What We Know About TMEM175 in Parkinson's Disease.CNS neuroscience & therapeutics · 2025Review
- Glucocerebrosidase deficiency leads to neuropathology via cellular immune activation.PLoS genetics · 2024Article
- Unraveling the Epigenetic Landscape: Insights into Parkinson's Disease, Amyotrophic Lateral Sclerosis, and Multiple Sclerosis.Brain sciences · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Neuroinflammation is one of the most significant factors involved in the initiation and progression of Parkinson's disease. PD is a neurodegenerative disorder with a motor disability linked with various complex and diversified risk factors. These factors trigger myriads of cellular and molecular processes, such as misfolding defective proteins, oxidative stress, mitochondrial dysfunction, and neurotoxic substances that induce selective neurodegeneration of dopamine neurons. This neuronal damage activates the neuronal immune system, including glial cells and inflammatory cytokines, to trigger neuroinflammation. The transition of acute to chronic neuroinflammation enhances the susceptibility of inflammation-induced dopaminergic neuron damage, forming a vicious cycle and prompting an individual to PD development. Epigenetic mechanisms recently have been at the forefront of the regulation of neuroinflammatory factors in PD, proposing a new dawn for breaking this vicious cycle. This review examined the core epigenetic mechanisms involved in the activation and phenotypic transformation of glial cells mediated neuroinflammation in PD. We found that epigenetic mechanisms do not work independently, despite being coordinated with each other to activate neuroinflammatory pathways. In this regard, we attempted to find the synergic correlation and contribution of these epigenetic modifications with various neuroinflammatory pathways to broaden the canvas of underlying pathological mechanisms involved in PD development. Moreover, this study highlighted the dual characteristics (neuroprotective/neurotoxic) of these epigenetic marks, which may counteract PD pathogenesis and make them potential candidates for devising future PD diagnosis and treatment.
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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.