Previously submitted to: JMIR Bioinformatics and Biotechnology (no longer under consideration since Dec 16, 2025)
Date Submitted: Oct 8, 2025
Warning: This is an author submission that is not peer-reviewed or edited. Preprints - unless they show as "accepted" - should not be relied on to guide clinical practice or health-related behavior and should not be reported in news media as established information.
Identification Of Key Genes And Pathways That Show A Connection Between Generalized Anxiety Disorder And Coronary Heart Disease: Study Using Bioinformatics.
ABSTRACT
Background:
Coronary heart disease develops when one’s arteries fill with plaque, causing decreased blood flow. Many people are at risk of this disease, including those of older age, those who smoke, or those with major mental health disorders. Additionally, anxiety disorders are caused by prolonged stress or worry. This research is important because coronary heart disease is the leading cause of death in the world; one study shows that it affects 126 million people globally. In addition, up to 33.7% of the population have been affected with some type of anxiety disorder in their lifetime.
Objective:
The objective of my research is to find genes or pathways that are common between people with both coronary heart disease and generalized anxiety disorder as potential targets for treatment. My hypothesis is that there are genes that are highly expressed in patients of both coronary heart disease and generalized anxiety disorder
Methods:
NCBI’s bioinformatics tool, GEO2R was used to analyze two datasets, one for coronary heart disease (GSE20686) and one for generalized anxiety disorder (GSE61672). The full table was downloaded to find the top 30 differentially expressed genes using p-value. SR Plot was used to further analyze the gene samples using GO and KEGG analysis.
Results:
The results revealed shared genes namely PLCL1 and DCX2, and overlapping biological pathways, including cytokine–cytokine receptor interaction and beta-catenin binding. These genes and pathways suggest a genetic connection and immune-related signaling that may help explain why anxiety can raise the risk of heart disease.
Conclusions:
This study showed that the most significant shared genes between the two diseases, ‘DCX2’ and ‘PLCL1’ and pathways, ‘Cytokine-cytokine receptor interaction’ and ‘beta-cantenin interaction’. point to a genetic overlap and immune/inflammatory signaling. This could explain why anxiety increases risk for heart disease. These genetic markers are potential therapeutic targets that researchers and clinicians might explore for future interventions addressing both conditions together. Clinical Trial: This was not a clinical trial, it was a bioinformatic study.
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