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Effects of doxorubicin-induced cardiotoxicity on cardiac mitochondrial dynamics and mitochondrial function: Insights for future interventions
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[1] Chiang Mai Univ, Dept Internal Med, Fac Med, Div Cardiol, Chiang Mai, Thailand
[2] Chiang Mai Univ, Cardiac Electrophysiol Res & Training Ctr, Fac Med, Chiang Mai 50200, Thailand
[3] Chiang Mai Univ, Ctr Excellence Cardiac Electrophysiol Res, Chiang Mai, Thailand
[4] Chiang Mai Univ, Cardiac Electrophysiol Unit, Dept Physiol, Fac Med, Chiang Mai, Thailand
关键词:
cardiotoxicity;
doxorubicin;
mitochondrial dynamics;
mitochondrial function;
INDUCED CARDIOMYOCYTE APOPTOSIS;
INDUCED OXIDATIVE STRESS;
FERRITIN HEAVY-CHAIN;
HEART-FAILURE;
CELL-DEATH;
RETROSPECTIVE ANALYSIS;
DYSFUNCTION;
INHIBITION;
METFORMIN;
TOXICITY;
D O I:
10.1111/jcmm.15305
中图分类号:
Q2 [细胞生物学];
学科分类号:
071009 ;
090102 ;
摘要:
Anthracyclines is an effective chemotherapeutic treatment used for many types of cancer. However, high cumulative dosage of anthracyclines leads to cardiac toxicity and heart failure. Dysregulation of mitochondrial dynamics and function are major pathways driving this toxicity. Several pharmacological and non-pharmacological interventions aiming to attenuate cardiac toxicity by targeting mitochondrial dynamics and function have shown beneficial effects in cell and animal models. However, in clinical practice, there is currently no standard therapy for the prevention of anthracycline-induced cardiotoxicity. This review summarizes current reports on the impact of anthracyclines on cardiac mitochondrial dynamics and mitochondrial function and potential interventions targeting these pathways. The roles of mitochondrial dynamics and mitochondrial function in the development of anthracycline-induced cardiotoxicity should provide insights in devising novel strategies to attenuate the cardiac toxicity induced by anthracyclines.
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页码:6534 / 6557
页数:24
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