ArticleJournal of inflammation research2024
A Neutrophil Extracellular Traps-Related Gene Trait Revealed the Prospective Therapy Strategy of Coronary Atherosclerosis.
Article in Journal of inflammation research, 2024. 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Exploring blood transcriptional signatures for thrombosis diagnosis in critically ill patients with COVID-19.Blood vessels, thrombosis & hemostasis · 2026Article
- Neutrophil Extracellular Traps: Potential Therapeutic Targets of Traditional Chinese Medicine and Natural Products for Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Exploring Endoplasmic Reticulum Stress-Related Genes in Cartilage Defects: Implications for Diagnosis and Therapy.Combinatorial chemistry & high throughput screening · 2026Article
- Association between leukocyte-derived composite indices and premature coronary artery disease: a cross-sectional study.BMC cardiovascular disorders · 2025Article
- Recent advances on the role of G0S2.Discover oncology · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Coronary atherosclerosis (CA) is a major cause of coronary artery disease (CHD), with inflammation significantly influencing its pathogenesis. This study explores the role of neutrophil extracellular traps (NETs) in CA to understand their influence on disease progression. Methods: Using the GEO database, we analyzed RNA expression microarray data from CA patients, identifying NET-related differentially expressed genes (NETDEGs) through logistic regression, SVM, and LASSO operator regression analyses. CA samples were categorized into risk subgroups based on gene traits, with further analysis on the biological characteristics and immune cell infiltration of the high-risk subgroup. Additionally, transcription factor (TF)-gene, microRNA (miRNA)-gene, and RNA binding protein (RBP)-gene regulatory networks were investigated, alongside a protein-drug network to propose potential targeting therapies. Expression levels of NETDEGs were validated via qRT-PCR and Western blotting. Results: Three NETDEGs-MMP9, ERN1, and G0S2-were pinpointed as key players in CA development, regulated by TFs, miRNAs, and RBPs. These genes defined high-risk subgroups marked by intense inflammatory signaling and apoptosis. High neutrophil infiltration correlated positively with NETDEG expression in CA samples, supporting their potential as biomarkers. MMP9 emerged as a notable drug target, providing a possible therapeutic avenue. Conclusion: This research highlights an independent NETDEG trait in CA, offering insights into potential biomarkers and therapeutic targets for combating this disease.
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