ArticleExperimental and therapeutic medicine2018
Smoking and drinking influence the advancing of ischemic stroke disease by targeting PTGS2 and TNFAIP3.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Passive smoking may be associated with bleeding of cerebral arteriovenous malformation in non-smoking women: a retrospective analysis.Arquivos de neuro-psiquiatria · 2022Article
- Exploring the Potential Mechanism of Shennao Fuyuan Tang for Ischemic Stroke Based on Network Pharmacology and Molecular Docking.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Bioinformatics Identification of Ferroptosis-Related Biomarkers and Therapeutic Compounds in Ischemic Stroke.Frontiers in neurology · 2021Article
- Role of Calcium Signaling Pathway-Related Gene Regulatory Networks in Ischemic Stroke Based on Multiple WGCNA and Single-Cell Analysis.Oxidative medicine and cellular longevity · 2021Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the present study, we explored the influence of cigarette smoking and alcohol drinking on gene expression level and related functions and pathways on the development of ischemic stroke (IS) disease. The gene expression profile of E-GEOD-22255 was obtained from 20 IS samples (7 patients without smoking or drinking history and 13 patients with smoking or drinking history) and 20 controls (9 normal controls without smoking or drinking history and 11 controls with smoking or drinking history). The correlation degree between gene expression and grouping were measured by significance analysis of microarray (SAM). Smoking or drinking-related DEGs were screened. GO functional and KEGG pathway enrichment analyses were processed. Based on the KEGG database, a pathway relationship network was constructed. DEGs in significant functions and pathways were inserted and regarded as key DEGs. Gene co-expression network was constructed based on the expression value of key genes. In total, 319 IS-related DEGs, which were induced by smoking and drinking, were screened and enriched in various functions and pathways, including inflammatory response, nuclear factor-κB (NF-κB) signaling pathway and influenza A. Pathway relationship network was constructed with 44 nodes and the hub node was the MAPK signaling pathway. After merging, 87 key DEGs were obtained. The gene co-expression network with 43 node edges was constructed and the hub node was prostaglandin-endoperoxide synthase 2. In IS patients, smoking and drinking may induce different expression of many genes, including
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