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Updated: Jul 3, 2026

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
Published on: May 16, 2020
Angiogenesis without functional outcome after mononuclear stem cell transplant in a doxorubicin-induced dilated
K A T Carvalho1, R B Simeoni, L C Guarita-Souza
1Pos-Graduacao de Ciencias da Saude da Universidade Pontificia Universidade Catolica do Parana', Curitiba, Parana' - Brazil. katherinecarv@gmail.com
Insights
Autologous mononuclear stem cell therapy did not improve heart function in rats with doxorubicin-induced cardiomyopathy. While new blood vessels formed, functional recovery was not observed in this preclinical study.
Area of Science:
- Cardiovascular Research
- Regenerative Medicine
- Stem Cell Therapy
Background:
- Dilated cardiomyopathy is a significant health concern.
- Doxorubicin chemotherapy can induce cardiotoxicity, leading to cardiomyopathy.
- Cell transplantation is being explored as a therapeutic strategy for heart disease.
Purpose of the Study:
- To assess the efficacy of autologous mononuclear stem cell therapy.
- To investigate the effects on doxorubicin-induced dilated cardiomyopathy in a rat model.
- To perform both functional and histopathological analyses.
Main Methods:
- Seventy male rats received doxorubicin, and those with reduced ejection fraction (<40%) were selected.
- Animals were divided into mononuclear stem cell therapy and control groups.
- Echocardiography was performed at baseline, pre-therapy, and 1 month post-therapy.
Main Results:
- Eleven rats completed the study (5 in cell group, 6 in control).
- Cell viability was 85%.
- No significant difference in left ventricular ejection fraction was observed between groups (p=0.54); however, new vessel formation was noted.
Conclusions:
- Autologous mononuclear stem cell therapy showed no functional benefit in this model of doxorubicin-induced cardiomyopathy.
- Angiogenic activity was observed despite the lack of functional improvement.
- Further research may be needed to optimize stem cell therapy for cardiac repair.
Objectives:
Cell transplantation is considered a novel approach in the treatment of myocardiopathy. The objective of this study was to evaluate the effects of autologous mononuclear stem cell therapy in doxorubicin-induced dilated myocardiopathy by conducting both functional and histopathologic analysis.
Methods:
Seventy male rats were doxorubicin injected intraperitoneally for 2 weeks. At 1 month, the animals that had demonstrated left ventricular ejection fractions less than 40% were randomly divided into a mononuclear stem cell group and controls. Mononuclear stem cells were isolated. All animals underwent echocardiographic study: baseline, pre-cell therapy, and at 1 month post-cell therapy, and analyzed by the nonparametric Mann-Whitney test. Transplants were performed by subepicardial injections. Standard staining was performed.
Results:
Twenty-three animals were randomly treated: mononuclear stem cell and control groups, with 11 rats completing the study. Cell viability was 85%. Mononuclear stem cells (n=5; 5x106 cells /300 microL medium) and control (n=6; 300 microL medium) were used. The resulting left ventricular ejection fraction in the cell therapy group was not significantly different compared with controls (p=0.54). New vessels were demonstrated in the subepicardial region.
Conclusions:
Autologous mononuclear stem cell therapy was not functionally effective in doxorubicin-induced dilated myocardiopathy in the animal model under study with the experimental conditions, despite occurrence of angiogenic activity.

