FTO ameliorates doxorubicin-induced cardiotoxicity by inhibiting ferroptosis via P53–P21/Nrf2 activation in a HuR-dependent m6A manner

FTO ameliorates doxorubicin-induced cardiotoxicity by inhibiting ferroptosis via P53–P21/Nrf2 activation in a HuR-dependent m6A manner

Doxorubicin (DOX)-induced cardiotoxicity seriously limits its clinical applicability, and no therapeutic interventions are available. Ferroptosis, an iron-dependent regulated cell death characterised by lipid peroxidation, plays a pivotal role in DOX-induced cardiotoxicity. N6-methyladenosine (m6A)...

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Bibliographic Details
Main Authors: Yunfan Yang, Jiajun Ren, Jifeng Zhang, Henghe Shi, Junnan Wang, Youyou Yan
Format: Article
Language:English
Published: Elsevier 2024-04-01
Series:Redox Biology
Subjects:
Doxorubicin
Ferroptosis
FTO
P53
P21
HuR
Online Access:http://www.sciencedirect.com/science/article/pii/S2213231724000430

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