Myeloperoxidase is a critical mediator of anthracycline-induced cardiomyopathy.
AICM
Cardiotoxicity
Doxorubicin
MPO
Polymorphonuclear neutrophils
Journal
Basic research in cardiology
ISSN: 1435-1803
Titre abrégé: Basic Res Cardiol
Pays: Germany
ID NLM: 0360342
Informations de publication
Date de publication:
01 09 2023
01 09 2023
Historique:
received:
31
10
2022
accepted:
24
08
2023
revised:
24
08
2023
medline:
4
9
2023
pubmed:
1
9
2023
entrez:
1
9
2023
Statut:
epublish
Résumé
Cardiotoxicity is a major complication of anthracycline therapy that negatively impacts prognosis. Effective pharmacotherapies for prevention of anthracycline-induced cardiomyopathy (AICM) are currently lacking. Increased plasma levels of the neutrophil-derived enzyme myeloperoxidase (MPO) predict occurrence of AICM in humans. We hypothesized that MPO release causally contributes to AICM. Mice intravenously injected with the anthracycline doxorubicin (DOX) exhibited higher neutrophil counts and MPO levels in the circulation and cardiac tissue compared to saline (NaCl)-treated controls. Neutrophil-like HL-60 cells exhibited increased MPO release upon exposition to DOX. DOX induced extensive nitrosative stress in cardiac tissue alongside with increased carbonylation of sarcomeric proteins in wildtype but not in Mpo
Identifiants
pubmed: 37656254
doi: 10.1007/s00395-023-01006-0
pii: 10.1007/s00395-023-01006-0
pmc: PMC10474188
doi:
Substances chimiques
Anthracyclines
0
Doxorubicin
80168379AG
Peroxidase
EC 1.11.1.7
MPO protein, human
EC 1.11.1.7
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
36Informations de copyright
© 2023. Springer-Verlag GmbH Germany, part of Springer Nature.
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