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Updated: May 31, 2025

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
Published on: June 7, 2018
Apelinergic System Affects Electrocardiographic Abnormalities Induced by Doxorubicin
Kasper Buczma1, Hubert Borzuta1, Katarzyna Kamińska1
1Chair and Department of Experimental and Clinical Physiology, Laboratory of Centre for Preclinical Research, Medical University of Warsaw, Banacha 1b, 02-097 Warsaw, Poland.
Apelin and elabela show promise in protecting against heart damage caused by chemotherapy drugs like doxorubicin (DOX). Lower doses of these agents can prevent or improve drug-induced cardiotoxicity in rats.
Area of Science:
- Cardiology
- Pharmacology
- Oncology
Background:
- Anthracyclines are vital chemotherapy drugs but cause significant cardiotoxicity.
- Developing cardioprotective strategies against anthracycline-induced cardiotoxicity is crucial.
- The apelinergic system's role in cardiovascular regulation makes it a potential target.
Purpose of the Study:
- To investigate the cardioprotective potential of the apelinergic system against doxorubicin (DOX)-induced cardiotoxicity.
- To evaluate the effects of apelin-13 and elabela on DOX-induced cardiac dysfunction.
Main Methods:
- 54 Sprague-Dawley rats were divided into seven groups.
- Rats received weekly intraperitoneal injections of DOX for 4 weeks.
- Apelin-13, elabela, or an APJ antagonist (ML221) were administered via osmotic pumps; controls received NaCl.
- Electrocardiography (ECG) and transthoracic echocardiography (TTE) were performed.
Main Results:
- Lower doses of APJ agonists (apelin-13, elabela) prevented DOX-induced QT and QTc interval prolongation.
- DOX administration led to left ventricular (LV) systolic dysfunction, confirmed by TTE.
- Simultaneous administration of APJ agonists improved LV systolic parameters in DOX-treated rats.
Conclusions:
- Apelin and elabela demonstrate potential as cardioprotective agents against anthracycline-induced cardiotoxicity.
- The findings suggest a therapeutic role for the apelinergic system in mitigating chemotherapy-related heart damage.
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