Related Experiment Video
Updated: Jul 18, 2025

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
Published on: June 7, 2018
Targeting mitochondrial dynamics proteins for the treatment of doxorubicin-induced cardiotoxicity
Rui Chen1, Mengwen Niu2, Xin Hu1
1Department of Cardiology, China-Japan Union Hospital of Jilin University, Changchun, China.
Abstract:
Doxorubicin (DOX) is an extensively used chemotherapeutic agent that can cause severe and frequent cardiotoxicity, which limits its clinical application. Although there have been extensive researches on the cardiotoxicity caused by DOX, there is still a lack of effective treatment. It is necessary to understand the molecular mechanism of DOX-induced cardiotoxicity and search for new therapeutic targets which do not sacrifice their anticancer effects. Mitochondria are considered to be the main target of cardiotoxicity caused by DOX. The imbalance of mitochondrial dynamics characterized by increased mitochondrial fission and inhibited mitochondrial fusion is often reported in DOX-induced cardiotoxicity, which can result in excessive ROS production, energy metabolism disorders, cell apoptosis, and various other problems. Also, mitochondrial dynamics disorder is related to tumorigenesis. Surprisingly, recent studies show that targeting mitochondrial dynamics proteins such as DRP1 and MFN2 can not only defend against DOX-induced cardiotoxicity but also enhance or not impair the anticancer effect. Herein, we summarize mitochondrial dynamics disorder in DOX-induced cardiac injury. Furthermore, we provide an overview of current pharmacological and non-pharmacological interventions targeting proteins involved in mitochondrial dynamics to alleviate cardiac damage caused by DOX.
Insights
Mitochondrial dynamics are key in doxorubicin (DOX) cardiotoxicity. Targeting proteins like DRP1 and MFN2 may protect the heart without reducing cancer treatment effectiveness.
Area of Science:
- Biochemistry
- Cardiology
- Oncology
Background:
- Doxorubicin (DOX) is a vital chemotherapy drug with dose-limiting cardiotoxicity.
- Mitochondria are primary targets of DOX-induced cardiac damage.
- Impaired mitochondrial dynamics (fission/fusion imbalance) contribute to DOX cardiotoxicity.
Purpose of the Study:
- To review mitochondrial dynamics in DOX cardiotoxicity.
- To explore therapeutic strategies targeting mitochondrial dynamics for DOX-induced cardiac injury.
- To assess if these strategies impact anticancer efficacy.
Main Methods:
- Literature review of studies on DOX cardiotoxicity and mitochondrial dynamics.
- Analysis of research on targeting mitochondrial dynamics proteins (e.g., DRP1, MFN2).
- Evaluation of interventions for DOX-induced cardiac damage.
Main Results:
- DOX disrupts mitochondrial dynamics, leading to ROS overproduction, metabolic dysfunction, and apoptosis.
- Targeting mitochondrial dynamics proteins shows promise in mitigating DOX cardiotoxicity.
- These interventions may preserve or even enhance DOX's anticancer effects.
Conclusions:
- Mitochondrial dynamics are a critical factor in DOX cardiotoxicity.
- Targeting mitochondrial dynamics offers a potential strategy to reduce cardiac side effects of DOX.
- Further research into these targets could lead to safer and more effective chemotherapy.
Related Concept Videos
Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...
Mitochondrial Membranes
Heart Failure Drugs: Inotropic Agents
Cardiomyopathy II: Dilated Cardiomyopathy

