Why the study?
Doxorubicin causes cardiotoxicity that limits its clinical use, and the roles and latent mechanisms of CYP2J2-derived epoxyeicosatrienoic acids in DOX cardiotoxicity remain uncertain.
Does CYP2J2 overexpression or EET pretreatment protect against doxorubicin-induced cardiotoxicity in preclinical models?
Population
C57BL/6J mice and H9C2 cell culture models
Comparison
rAAV9-CYP2J2 vs control vector in vivo; 14,15-EET pretreatment vs no pretreatment in vitro
Design
Preclinical animal and in vitro cell culture study
Authors
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CYP2J2/EETs may protect against doxorubicin cardiotoxicity in mice; leaves open clinical translation pending human studies.
Does CYP2J2 overexpression or EET pretreatment protect against doxorubicin-induced cardiotoxicity in preclinical models?
CYP2J2-derived EETs protect against doxorubicin-induced cardiotoxicity by activating the AMPK pathway, suggesting a potential therapeutic target for chemotherapy-induced cardiomyopathy.
Zhu et al. (2023) studied this question.
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