Heat Shock Protein 22 Attenuates Doxorubicin-Induced Cardiotoxicity
Hsp22
TLR/NLRP3
apoptosis
doxorubicin
inflammation
Journal
Frontiers in pharmacology
ISSN: 1663-9812
Titre abrégé: Front Pharmacol
Pays: Switzerland
ID NLM: 101548923
Informations de publication
Date de publication:
2020
2020
Historique:
received:
06
10
2019
accepted:
24
02
2020
entrez:
10
4
2020
pubmed:
10
4
2020
medline:
10
4
2020
Statut:
epublish
Résumé
The antitumor effect of doxorubicin (DOX) is limited by its acute and chronic toxicity to the heart, which causes heart injury. Heat shock protein 22 (Hsp22) is a protein proved to exert anti-apoptosis and anti-inflammatory effects in other diseases and physical conditions. In this study, we aim to explore whether Hsp22 could exert a protective role during cardiac injury in response to DOX. The overexpression of Hsp22 was mediated An increase in the expression level of Hsp22 was observed in DOX-treated heart tissue. Furthermore, cardiac-specific overexpression of Hsp22 showed reduced cardiac dysfunction, decrease in inflammatory response, and reduction in cell apoptosis in injury heart and cardiomyocytes induced by DOX In summary, Hsp22 overexpression in the heart could suppress cardiac injury in response to DOX treatment through blocking TLR4/NLRP3 activation. Hsp22 may become a new therapeutic method for treating cardiac injury induced by DOX in cancer patients.
Sections du résumé
BACKGROUND
BACKGROUND
The antitumor effect of doxorubicin (DOX) is limited by its acute and chronic toxicity to the heart, which causes heart injury. Heat shock protein 22 (Hsp22) is a protein proved to exert anti-apoptosis and anti-inflammatory effects in other diseases and physical conditions. In this study, we aim to explore whether Hsp22 could exert a protective role during cardiac injury in response to DOX.
METHODS
METHODS
The overexpression of Hsp22 was mediated
RESULTS
RESULTS
An increase in the expression level of Hsp22 was observed in DOX-treated heart tissue. Furthermore, cardiac-specific overexpression of Hsp22 showed reduced cardiac dysfunction, decrease in inflammatory response, and reduction in cell apoptosis in injury heart and cardiomyocytes induced by DOX
CONCLUSION
CONCLUSIONS
In summary, Hsp22 overexpression in the heart could suppress cardiac injury in response to DOX treatment through blocking TLR4/NLRP3 activation. Hsp22 may become a new therapeutic method for treating cardiac injury induced by DOX in cancer patients.
Identifiants
pubmed: 32269523
doi: 10.3389/fphar.2020.00257
pmc: PMC7109316
doi:
Types de publication
Journal Article
Langues
eng
Pagination
257Informations de copyright
Copyright © 2020 Lan, Wang, Huang and Zeng.
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