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Updated: Sep 15, 2025
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A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
Published on: May 16, 2020
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Integrating Microarray Analysis, Machine Learning, and Molecular Docking to Explore the Mechanism of
Yidong Zhu1, Jun He2, Rong Wei2
1Department of Traditional Chinese Medicine, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Current Medicinal Chemistry
|July 17, 2025
Summary
Doxorubicin (DOX) chemotherapy causes cardiotoxicity due to poorly understood mechanisms. This study identified five key genes and pathways, including Rap1 signaling, offering insights for safer cancer treatments.
Area of Science:
- Cardiotoxicity research
- Chemotherapeutic drug safety
- Molecular toxicology
Background:
- Doxorubicin (DOX) is a vital chemotherapy drug, but its use is limited by cardiotoxicity.
- The molecular basis of DOX-induced cardiotoxicity is not fully understood, hindering effective interventions.
- Identifying key molecular targets is crucial for developing strategies to mitigate DOX cardiotoxicity.
Purpose of the Study:
- To identify core target genes implicated in Doxorubicin-induced cardiotoxicity.
- To explore the molecular mechanisms underlying Doxorubicin-induced cardiotoxicity.
- To integrate multi-omics and computational approaches for toxicological pathway discovery.
Main Methods:
- Differential gene expression analysis of microarray data from DOX-treated samples.
- Application of machine learning algorithms (e.g., Support Vector Machine) to identify critical genes.
- Molecular docking simulations to assess drug-target interactions and functional pathway analysis.
Main Results:
- Identified 276 differentially expressed genes in DOX cardiotoxicity.
- Discovered five core target genes (RAP1A, CTLA4, OR2M1P, TRIM53, LOC149837) with high predictive power (AUC > 0.85).
- Revealed stable binding of DOX to target genes and suggested involvement of Rap1 signaling and immune regulation.
Conclusions:
- Integrated bioinformatics approaches provide a robust framework for understanding complex toxicological mechanisms.
- The identified genes and pathways offer novel insights into DOX-induced cardiotoxicity.
- Findings support the development of targeted protective strategies against Doxorubicin cardiotoxicity.
