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December 9, 2023HeliyonOpen Access

CYP2J2 overexpression and 14,15-EET mitigated DOX-induced cardiotoxicity, diminished cardiac injury markers, improved heart function, and reduced oxidative stress and apoptosis via AMPK pathway activation.

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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

CZChuanmeng ZhuYBYang BaiJQJie Qiu

Discussion

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Member takes

Overview

CYP2J2/EETs may protect against doxorubicin cardiotoxicity in mice; leaves open clinical translation pending human studies.

Structured PICO

Does CYP2J2 overexpression or EET pretreatment protect against doxorubicin-induced cardiotoxicity in preclinical models?

P
Population
C57BL/6J mice and H9C2 cell culture models of doxorubicin-induced cardiotoxicity
I
Intervention
CYP2J2 overexpression via rAAV9-CYP2J2 injection (in vivo) or 14,15-EET pretreatment (in vitro)
C
Comparator
Control vector (in vivo) or no pretreatment (in vitro)
O
Outcome
Doxorubicin-induced cardiotoxicity (cardiac injury markers, heart function, oxidative stress, and myocardial apoptosis)surrogate

CYP2J2-derived EETs protect against doxorubicin-induced cardiotoxicity by activating the AMPK pathway, suggesting a potential therapeutic target for chemotherapy-induced cardiomyopathy.

Cite This Study

Zhu et al. (2023) studied this question.

synapsesocial.com/papers/6a796a2602ab7a73dd02558ahttps://doi.org/10.1016/j.heliyon.2023.e23526
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Overexpression of CYP2J2 provides protection against doxorubicin-induced cardiotoxicity2009 · 94 citations
  2. 2O74 EPOXYEICOSATRIENOIC ACIDS ANALOGUE (EET-A) FOR THE TREATMENT OF CHEMOTHERAPY-INDUCED HEART FAILURE WITH NEPHROTIC SYNDROME2024
  3. 3CYP2J2 and EETs Protect against Oxidative Stress and Apoptosisin Vivoandin VitroFollowing Lung Ischemia/Reperfusion2014 · 58 citations
  4. 42-Methoxyestradiol ameliorates doxorubicin-induced cardiotoxicity by regulating the expression of GLUT4 and CPT-1B in female rats2024 · 3 citations
  5. 5<scp>CYP</scp> 2J2 and its metabolites (epoxyeicosatrienoic acids) attenuate cardiac hypertrophy by activating <scp>AMPK</scp> α2 and enhancing nuclear translocation of Akt12016 · 41 citations