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Microglial Activation and Oxidative Stress in PM(2.5)-Induced Neurodegenerative Disorders
Fine particulate matter (PM(2.5)) pollution remains a prominent environmental problem worldwide, posing great threats to human health. The adverse effects of PM(2.5) on the respiratory and cardiovascular systems have been extensively studied, while its detrimental effects on the central nervous syst...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9404971/ https://www.ncbi.nlm.nih.gov/pubmed/36009201 http://dx.doi.org/10.3390/antiox11081482 |
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author | Song, Jie Han, Keyang Wang, Ya Qu, Rongrong Liu, Yuan Wang, Shaolan Wang, Yinbiao An, Zhen Li, Juan Wu, Hui Wu, Weidong |
author_facet | Song, Jie Han, Keyang Wang, Ya Qu, Rongrong Liu, Yuan Wang, Shaolan Wang, Yinbiao An, Zhen Li, Juan Wu, Hui Wu, Weidong |
author_sort | Song, Jie |
collection | PubMed |
description | Fine particulate matter (PM(2.5)) pollution remains a prominent environmental problem worldwide, posing great threats to human health. The adverse effects of PM(2.5) on the respiratory and cardiovascular systems have been extensively studied, while its detrimental effects on the central nervous system (CNS), specifically neurodegenerative disorders, are less investigated. Neurodegenerative disorders are characterized by reduced neurogenesis, activated microglia, and neuroinflammation. A variety of studies involving postmortem examinations, epidemiological investigations, animal experiments, and in vitro cell models have shown that PM(2.5) exposure results in neuroinflammation, oxidative stress, mitochondrial dysfunction, neuronal apoptosis, and ultimately neurodegenerative disorders, which are strongly associated with the activation of microglia. Microglia are the major innate immune cells of the brain, surveilling and maintaining the homeostasis of CNS. Upon activation by environmental and endogenous insults, such as PM exposure, microglia can enter an overactivated state that is featured by amoeboid morphology, the over-production of reactive oxygen species, and pro-inflammatory mediators. This review summarizes the evidence of microglial activation and oxidative stress and neurodegenerative disorders following PM(2.5) exposure. Moreover, the possible mechanisms underlying PM(2.5)-induced microglial activation and neurodegenerative disorders are discussed. This knowledge provides certain clues for the development of therapies that may slow or halt the progression of neurodegenerative disorders induced by ambient PM. |
format | Online Article Text |
id | pubmed-9404971 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-94049712022-08-26 Microglial Activation and Oxidative Stress in PM(2.5)-Induced Neurodegenerative Disorders Song, Jie Han, Keyang Wang, Ya Qu, Rongrong Liu, Yuan Wang, Shaolan Wang, Yinbiao An, Zhen Li, Juan Wu, Hui Wu, Weidong Antioxidants (Basel) Review Fine particulate matter (PM(2.5)) pollution remains a prominent environmental problem worldwide, posing great threats to human health. The adverse effects of PM(2.5) on the respiratory and cardiovascular systems have been extensively studied, while its detrimental effects on the central nervous system (CNS), specifically neurodegenerative disorders, are less investigated. Neurodegenerative disorders are characterized by reduced neurogenesis, activated microglia, and neuroinflammation. A variety of studies involving postmortem examinations, epidemiological investigations, animal experiments, and in vitro cell models have shown that PM(2.5) exposure results in neuroinflammation, oxidative stress, mitochondrial dysfunction, neuronal apoptosis, and ultimately neurodegenerative disorders, which are strongly associated with the activation of microglia. Microglia are the major innate immune cells of the brain, surveilling and maintaining the homeostasis of CNS. Upon activation by environmental and endogenous insults, such as PM exposure, microglia can enter an overactivated state that is featured by amoeboid morphology, the over-production of reactive oxygen species, and pro-inflammatory mediators. This review summarizes the evidence of microglial activation and oxidative stress and neurodegenerative disorders following PM(2.5) exposure. Moreover, the possible mechanisms underlying PM(2.5)-induced microglial activation and neurodegenerative disorders are discussed. This knowledge provides certain clues for the development of therapies that may slow or halt the progression of neurodegenerative disorders induced by ambient PM. MDPI 2022-07-29 /pmc/articles/PMC9404971/ /pubmed/36009201 http://dx.doi.org/10.3390/antiox11081482 Text en © 2022 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 Song, Jie Han, Keyang Wang, Ya Qu, Rongrong Liu, Yuan Wang, Shaolan Wang, Yinbiao An, Zhen Li, Juan Wu, Hui Wu, Weidong Microglial Activation and Oxidative Stress in PM(2.5)-Induced Neurodegenerative Disorders |
title | Microglial Activation and Oxidative Stress in PM(2.5)-Induced Neurodegenerative Disorders |
title_full | Microglial Activation and Oxidative Stress in PM(2.5)-Induced Neurodegenerative Disorders |
title_fullStr | Microglial Activation and Oxidative Stress in PM(2.5)-Induced Neurodegenerative Disorders |
title_full_unstemmed | Microglial Activation and Oxidative Stress in PM(2.5)-Induced Neurodegenerative Disorders |
title_short | Microglial Activation and Oxidative Stress in PM(2.5)-Induced Neurodegenerative Disorders |
title_sort | microglial activation and oxidative stress in pm(2.5)-induced neurodegenerative disorders |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9404971/ https://www.ncbi.nlm.nih.gov/pubmed/36009201 http://dx.doi.org/10.3390/antiox11081482 |
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