ArticleFrontiers in cardiovascular medicine2023
Identification of common signature genes and pathways underlying the pathogenesis association between nonalcoholic fatty liver disease and atherosclerosis.
Article in Frontiers in cardiovascular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Diagnostic Value of Oxidative Stress-Related Features Mined by WGCNA and Machine Learning in Respiratory Syncytial Virus Infection.Advanced biology · 2026Article
- Identifying and Diagnosing Lytic Cell Death Genes in Atherosclerosis Using Machine Learning and Bioinformatics.Journal of inflammation research · 2025Article
- Identification of biomarkers between coronary artery disease and non-alcoholic steatohepatitis: a combination of bioinformatics and machine learning.Frontiers in genetics · 2025Article
- Integrative Analyses of Genes of Pediatric Non-alcoholic Fatty Liver Disease Associated with Energy Metabolism.Digestive diseases and sciences · 2024Article
- Causal relationships between three plasma proteins and non-alcoholic fatty liver disease, mediated by Epstein-Barr virus EA-D antibody levels: a mendelian randomization study.Scientific reports · 2024Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Atherosclerosis (AS) is one of the leading causes of the cardio-cerebral vascular incident. The constantly emerging evidence indicates a close association between nonalcoholic fatty liver disease (NAFLD) and AS. However, the exact molecular mechanisms underlying the correlation between these two diseases remain unclear. This study proposed exploring the common signature genes, pathways, and immune cells among AS and NAFLD. Methods: The common differentially expressed genes (co-DEGs) with a consistent trend were identified Results: A total of 11 co-DEGs were identified. GO and KEGG analyses revealed that co-DEGs were mainly enriched in lipid catabolic process, calcium ion transport, and regulation of cytokine. Moreover, three common signature genes (PLCXD3, CCL19, and PKD2) were defined. Based on these genes, we constructed the efficiently predictable diagnostic models for advanced AS and NAFLD with the nomograms, evaluated with the ROC curves (AUC = 0.995 for advanced AS, 95% CI 0.971-1.0; AUC = 0.973 for advanced NAFLD, 95% CI 0.938-0.998). In addition, the AUC of the verification datasets had a similar trend. The NOD-like receptors (NLRs) signaling pathway might be the most crucial co-regulated pathway, and activated CD4 T cells and central memory CD4 T cells were significantly excessive infiltration in advanced NAFLD and AS. Conclusion: We identified three common signature genes (PLCXD3, CCL19, and PKD2), co-regulated pathways, and shared immune features of NAFLD and AS, which might provide novel insights into the molecular mechanism of NAFLD complicated with AS.
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