ArticleHeliyon2024
Comprehensive analysis of shared risk genes and immunity-metabolisms between non-alcoholic fatty liver disease and atherosclerosis via bulk and single-cell transcriptome analyses.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- [Dual role and therapeutic potential of TREM2 in atherosclerosis].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Review
- Discrimination of Steatotic and Non-Steatotic Chemicals Through Transcriptome Analysis in Primary Human Hepatocytes.International journal of molecular sciences · 2026Article
- Risk-associated and clinically informative biomarkers for cardiovascular risk stratification in metabolic dysfunction-Associated steatotic liver disease.American journal of preventive cardiology · 2026Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: and design: Considering the clinical link between non-alcoholic fatty liver disease (NAFLD) and atherosclerosis (AS), we performed bioinformatics analysis to uncover their pathogenic interrelationship. Methods and results: Data from the U.S. National Health and Nutritional Examination Survey (NHANES) 1999-2018 were included. Among 4851 participants in NHANES, NAFLD was significantly associated with atherosclerotic cardiovascular disease risk (ASCVD risk) (OR = 2.32, 95%CI: 2.04-2.65, P < 0.0001). We conducted WGCNA analysis for NAFLD (GSE130970) and AS (GSE28829) and identified three modules positively related to NAFLD severity and two modules accelerating atherosclerosis plaque progression. 198 key-modules genes were obtained via overlapping these modules. Next, we mined the disease-controlled differentially expressed genes (DEGs) from NAFLD (GSE89632) and AS (GSE100927), respectively. The final common risk genes ( Conclusion: We found 7 shared hub genes with good diagnostic ability and depicted the landscapes of immune and metabolism involved in NAFLD and AS. Our results provided a comprehensive association between them and may contribute to developing potential intervention strategies for targeting both disorders based on these risk factors.
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Registered trials
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