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Epigenetic Regulation of Neuroinflammation in Parkinson’s Disease
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 pro...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8125491/ https://www.ncbi.nlm.nih.gov/pubmed/34066949 http://dx.doi.org/10.3390/ijms22094956 |
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author | Rasheed, Madiha Liang, Junhan Wang, Chaolei Deng, Yulin Chen, Zixuan |
author_facet | Rasheed, Madiha Liang, Junhan Wang, Chaolei Deng, Yulin Chen, Zixuan |
author_sort | Rasheed, Madiha |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-8125491 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-81254912021-05-17 Epigenetic Regulation of Neuroinflammation in Parkinson’s Disease Rasheed, Madiha Liang, Junhan Wang, Chaolei Deng, Yulin Chen, Zixuan Int J Mol Sci Review 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. MDPI 2021-05-07 /pmc/articles/PMC8125491/ /pubmed/34066949 http://dx.doi.org/10.3390/ijms22094956 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Rasheed, Madiha Liang, Junhan Wang, Chaolei Deng, Yulin Chen, Zixuan Epigenetic Regulation of Neuroinflammation in Parkinson’s Disease |
title | Epigenetic Regulation of Neuroinflammation in Parkinson’s Disease |
title_full | Epigenetic Regulation of Neuroinflammation in Parkinson’s Disease |
title_fullStr | Epigenetic Regulation of Neuroinflammation in Parkinson’s Disease |
title_full_unstemmed | Epigenetic Regulation of Neuroinflammation in Parkinson’s Disease |
title_short | Epigenetic Regulation of Neuroinflammation in Parkinson’s Disease |
title_sort | epigenetic regulation of neuroinflammation in parkinson’s disease |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8125491/ https://www.ncbi.nlm.nih.gov/pubmed/34066949 http://dx.doi.org/10.3390/ijms22094956 |
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