Airway hyperresponsiveness development and the toxicity of PM2.5.
Airway hyperresponsiveness
Asthma
Autophagy
Cell cycle alteration
Cytoplasmic calcium concentration Apoptosis
Epigenetic alterations
Fine particulate matter (PM2.5)
Immune system imbalances
Inflammatory responses
Oxidative stress
Journal
Environmental science and pollution research international
ISSN: 1614-7499
Titre abrégé: Environ Sci Pollut Res Int
Pays: Germany
ID NLM: 9441769
Informations de publication
Date de publication:
Feb 2021
Feb 2021
Historique:
received:
07
07
2020
accepted:
10
12
2020
pubmed:
5
1
2021
medline:
30
1
2021
entrez:
4
1
2021
Statut:
ppublish
Résumé
Airway hyperresponsiveness (AHR) is characterized by excessive bronchoconstriction in response to nonspecific stimuli, thereby leading to airway stenosis and increased airway resistance. AHR is recognized as a key characteristic of asthma and is associated with significant morbidity. At present, many studies on the molecular mechanisms of AHR have mainly focused on the imbalance in Th1/Th2 cell function and the abnormal contraction of airway smooth muscle cells. However, the specific mechanisms of AHR remain unclear and need to be systematically elaborated. In addition, the effect of air pollution on the respiratory system has become a worldwide concern. To date, numerous studies have indicated that certain concentrations of fine particulate matter (PM2.5) can increase airway responsiveness and induce acute exacerbation of asthma. Of note, the concentration of PM2.5 does correlate with the degree of AHR. Numerous studies exploring the toxicity of PM2.5 have mainly focused on the inflammatory response, oxidative stress, genotoxicity, apoptosis, autophagy, and so on. However, there have been few reviews systematically elaborating the molecular mechanisms by which PM2.5 induces AHR. The present review separately sheds light on the underlying molecular mechanisms of AHR and PM2.5-induced AHR.
Identifiants
pubmed: 33394441
doi: 10.1007/s11356-020-12051-w
pii: 10.1007/s11356-020-12051-w
doi:
Substances chimiques
Particulate Matter
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
6374-6391Références
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