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Updated: Jun 6, 2025

Behavioral and Network Pharmacology-Based Analyses for the Traditional Mongolian Medicine Zadi-5 in a Rat Model of Depression
Published on: February 24, 2023
Unveiling shared therapeutic targets and pathological pathways between coronary artery disease and major depressive
Mengyun Hu1, Rong Tan1, Caihong Lu2
1Department of Nursing, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, Hubei Province, China.
Insights
This study identifies shared molecular mechanisms between coronary artery disease (CAD) and major depressive disorder (MDD). Key genes CDC42, NDUFB3, and TXN show potential as biomarkers and therapeutic targets for treating both conditions concurrently.
Area of Science:
- Genomics
- Cardiovascular Medicine
- Psychiatry
Background:
- Coronary artery disease (CAD) and major depressive disorder (MDD) are significant health concerns.
- Understanding shared biological mechanisms between CAD and MDD is crucial for developing integrated treatments.
Purpose of the Study:
- To identify common differentially expressed genes (DEGs) and pathways between CAD and MDD.
- To validate potential hub genes and discover therapeutic targets for co-treatment.
Main Methods:
- Differential gene expression analysis, functional enrichment, and Protein-Protein Interaction network construction.
- Gene co-expression network analysis, immune cell infiltration assessment, and molecular docking.
Main Results:
- Overlapping DEGs were enriched in Herpes simplex virus 1 infection and NF-kappa B signaling pathways.
- CDC42, NDUFB3, and TXN were identified as key hub genes associated with CAD.
- GS-9620 emerged as a potential drug candidate targeting these shared pathways.
Conclusions:
- CDC42, NDUFB3, and TXN represent promising molecular biomarkers for CAD and MDD.
- These genes offer potential therapeutic targets for simultaneous treatment of cardiovascular and depressive disorders.
Abstract:
Coronary artery disease (CAD) is a predominant cardiovascular condition influenced by risk factors, with an emphasis on major depressive disorder (MDD). However, the shared mechanisms and therapeutic targets for CAD and MDD remain incompletely comprehended. Functional enrichment analyses were conducted to investigate the pathways associated with the differentially expressed genes (DEGs) in the CAD and MDD datasets. Hub genes were identified utilizing the Protein-Protein Interaction network and Cytoscape software. The single sample gene set variation analysis was applied to assess immune cell infiltration in the CAD and MDD datasets. Weighted gene co-expression network analysis and molecular biological experiments were executed to evaluate these hub genes. Molecular docking was conducted to identify drug candidates targeting these hub genes. The overlapping DEGs between the CAD and MDD datasets were mainly enriched in the Herpes simplex virus 1 infection and the NF-kappa B signaling pathways. CDC42, NDUFB3, and TXN were validated within the eigengenes of the blue module, which exhibited a significant association with the CAD phenotype. The drug candidate GS-9620 was identified as a potential protective agent against both disorders. In conclusion, CDC42, NDUFB3, and TXN held potential as molecular biomarkers and therapeutic targets for the simultaneous treatment of CAD and MDD.
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