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NRF2 upregulation by CDDO-Me protects AC16 human cardiomyocytes against doxorubicin-induced toxicity

delete2025-12-18
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OA
AI
J
James A. Roberts *
M
Michael Batie
A
Amy H. Ponsford
J
Jonathan Poh
B
Benjamin J. Hewitt
H
Hannah F. Botfield
L
Lisa J. Hill
C
Christopher M. Sanderson
S
Sónia Rocha
P
Parveen Sharma *
DOI：10.1016/j.biopha.2025.118878delete
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Abstract

Abstract

En 中文
• CDDO-Me induces a rapid and sustained NRF2 response in human cardiomyocytes. • Genetic and pharmacological NRF2 activation diminishes doxorubicin cardiotoxicity. • CDDO-Me inhibits doxorubicin cardiotoxicity without affecting anticancer efficacy. • CDDO-Me decreases doxorubicin-induced oxidative stress, cell death and fibrosis.
Keywords:
NRF2
Doxorubicin
Oxidative stress
RNA-seq
Cardiotoxicity
Antioxidant
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Journal

B
Biomedicine and Pharmacotherapy
IF:
7.5
Papers:
1.6W
Citations:
8.2W

Organization

U
University of Birmingham
Scholars:
4.1W
Papers: 3.8W
Citations: 5.0W
U
University of Liverpool
Scholars:
2.8W
Papers: 2.5W
Citations: 3.5W
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