Endocrine, metabolic & immune disorders drug targets · 2026
Integrated Bioinformatics Analysis of Autophagy-Related Biomarkers in Atherosclerosis and Acquired Immune Deficiency Syndrome.
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Zhong Hua, Zhang Fangfang, Wu Yupeng, Zhang Yuzhu, Sha Anxiang, Zhu Zaihan, Bao Min, Sun Dandan
Аннотация
INTRODUCTION: Atherosclerosis (AS) and acquired immune deficiency syndrome (AIDS) are associated with autophagy-related pathways. This research was intended to ascertain the interplay between AS and AIDS through autophagy-related mechanisms and to identify potential common biomarkers.
METHODS: Single-cell datasets for AS and AIDS were extracted from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) from each dataset were identified and then intersected with autophagy-related genes (ATGs). Functional enrichment and protein-protein interaction (PPI) network analyses were performed. Hub genes were determined via CytoHubba and MCODE. Finally, the hub genes were validated via bulk transcriptomic data. ROC curves were plotted, and their correlations with immune cell infiltration were investigated. Transcription factor networks and drug-gene interactions were implemented.
RESULTS: 17 key ATGs were found, which were primarily enriched in autophagy, apoptosis, and TGF-β signaling pathways. After intersecting the 17 ATGs with DEGs using four algorithms in the Cytoscape plugin, eight genes were identified. Finally, three hub genes, encompassing GAPDH, HSPA8, and REL, were determined. ROC curves confirmed their diagnostic value. Their expression levels were markedly correlated with immune cell infiltration, and potential drugs were forecast.
DISCUSSION: This study demonstrates that GAPDH, HSPA8, and REL form a shared molecular pathway linking AS and AIDS via dysregulated autophagy, highlighting their potential as diagnostic biomarkers and therapeutic targets.
CONCLUSION: Three hub genes, including GAPDH, HSPA8, and REL, were determined as potential biomarkers for AIDS and AS, providing insights into the molecular mechanisms of HIV-associated AS.
METHODS: Single-cell datasets for AS and AIDS were extracted from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) from each dataset were identified and then intersected with autophagy-related genes (ATGs). Functional enrichment and protein-protein interaction (PPI) network analyses were performed. Hub genes were determined via CytoHubba and MCODE. Finally, the hub genes were validated via bulk transcriptomic data. ROC curves were plotted, and their correlations with immune cell infiltration were investigated. Transcription factor networks and drug-gene interactions were implemented.
RESULTS: 17 key ATGs were found, which were primarily enriched in autophagy, apoptosis, and TGF-β signaling pathways. After intersecting the 17 ATGs with DEGs using four algorithms in the Cytoscape plugin, eight genes were identified. Finally, three hub genes, encompassing GAPDH, HSPA8, and REL, were determined. ROC curves confirmed their diagnostic value. Their expression levels were markedly correlated with immune cell infiltration, and potential drugs were forecast.
DISCUSSION: This study demonstrates that GAPDH, HSPA8, and REL form a shared molecular pathway linking AS and AIDS via dysregulated autophagy, highlighting their potential as diagnostic biomarkers and therapeutic targets.
CONCLUSION: Three hub genes, including GAPDH, HSPA8, and REL, were determined as potential biomarkers for AIDS and AS, providing insights into the molecular mechanisms of HIV-associated AS.