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Updated: Feb 20, 2026

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
Published on: June 7, 2018
Molecular mechanism of doxorubicin-induced cardiomyopathy - An update
Kaviyarasi Renu1, Abilash V G1, Tirupathi Pichiah P B2
1Department of Biomedical Sciences, School of Biosciences and Technology, VIT University, Vellore, Tamil Nadu 632014, India.
Abstract:
Doxorubicin is utilized for anti-neoplastic treatment for several decades. The utility of this drug is limited due to its side effects. Generally, doxorubicin toxicity is originated from the myocardium and then other organs are also ruined. The mechanism of doxorubicin is intercalated with the DNA and inhibits topoisomerase 2. There are various signalling mechanisms involved in doxorubicin cardiotoxicity. First and foremost, the doxorubicin-induced cardiotoxicity is due to oxidative stress. Cardiac mitochondrial damage is supposed after few hours following the revelation of doxorubicin. This has led important new uses for the mechanism of doxorubicin-induced cardiotoxicity and novel avenues of investigation to determine better pharmacotherapies and interventions for the impediment of cardiotoxicity. The idea of this review is to bring up to date the recent findings of the mechanism of doxorubicin cardiomyopathies such as calcium dysregulation, endoplasmic reticulum stress, impairment of progenitor cells, activation of immune, ubiquitous system and some other parameters.
Insights
Doxorubicin, a chemotherapy drug, causes heart damage (cardiotoxicity) through mechanisms like oxidative stress. This review updates findings on doxorubicin cardiomyopathies to find better treatments.
Area of Science:
- Oncology
- Cardiology
- Pharmacology
Background:
- Doxorubicin is a widely used anti-neoplastic agent.
- Its clinical utility is significantly limited by dose-dependent cardiotoxicity.
- Cardiotoxicity affects the myocardium and other organs, impacting patient outcomes.
Purpose of the Study:
- To provide an updated review of the mechanisms underlying doxorubicin-induced cardiotoxicity and cardiomyopathies.
- To highlight recent findings and novel avenues for therapeutic interventions.
- To consolidate current knowledge on doxorubicin's detrimental effects on the heart.
Main Methods:
- Literature review of recent scientific findings on doxorubicin cardiotoxicity.
- Analysis of signaling pathways involved in doxorubicin-induced cardiac damage.
- Synthesis of information on emerging therapeutic strategies.
Main Results:
- Doxorubicin exerts its anti-cancer effect by DNA intercalation and topoisomerase 2 inhibition.
- Key mechanisms of cardiotoxicity include oxidative stress and cardiac mitochondrial damage.
- Other contributing factors identified are calcium dysregulation, endoplasmic reticulum stress, progenitor cell impairment, and immune system activation.
Conclusions:
- Understanding the multifaceted mechanisms of doxorubicin cardiotoxicity is crucial for developing effective interventions.
- Targeting pathways such as oxidative stress and calcium dysregulation may mitigate cardiac damage.
- Further research into novel pharmacotherapies is essential to improve the safety profile of doxorubicin treatment.
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