Article ; Online: Inhibition of METTL3 ameliorates doxorubicin-induced cardiotoxicity through suppression of TFRC-mediated ferroptosis.
2024 Volume 72, Page(s) 103157
Abstract: Background: Doxorubicin (DOX) is a chemotherapeutic drug, while its clinical use is greatly limited by the life-threatening cardiotoxicity. N: Methods: Mice were administrated with DOX (accumulative dosage of 20 mg/kg) repeatedly to establish a ... ...
Abstract | Background: Doxorubicin (DOX) is a chemotherapeutic drug, while its clinical use is greatly limited by the life-threatening cardiotoxicity. N Methods: Mice were administrated with DOX (accumulative dosage of 20 mg/kg) repeatedly to establish a chronic DIC model. Cardiomyocyte-specific conditional METTL3 knockout mice were employed to evaluate the effects of altered m Results: DOX led to increased levels in m Conclusion: METTL3 plays a cardinal role in the etiology of DIC by regulating cardiac iron metabolism and ferroptosis through TFRC m |
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MeSH term(s) | Animals ; Mice ; Doxorubicin/adverse effects ; Cardiotoxicity/etiology ; Cardiotoxicity/metabolism ; Methyltransferases/metabolism ; Methyltransferases/genetics ; Ferroptosis/drug effects ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/drug effects ; Mice, Knockout ; Adenosine/analogs & derivatives ; Adenosine/metabolism ; Male ; Humans |
Chemical Substances | Doxorubicin (80168379AG) ; Methyltransferases (EC 2.1.1.-) ; Mettl3 protein, mouse (EC 2.1.1.-) ; Adenosine (K72T3FS567) ; N-methyladenosine (CLE6G00625) |
Language | English |
Publishing date | 2024-04-12 |
Publishing country | Netherlands |
Document type | Journal Article ; Research Support, Non-U.S. Gov't |
ZDB-ID | 2701011-9 |
ISSN | 2213-2317 ; 2213-2317 |
ISSN (online) | 2213-2317 |
ISSN | 2213-2317 |
DOI | 10.1016/j.redox.2024.103157 |
Database | MEDical Literature Analysis and Retrieval System OnLINE |
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