Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atherosclerosis remains a leading cause of morbidity and mortality worldwide. In addition to the deposition of cholesterol in the arterial wall, inflammation, cell proliferation and migration play important roles in the pathogenesis of atherosclerosis. Thrombomodulin (TM) is a cell surface-expressed glycoprotein which is predominantly synthesized by vascular endothelial cells and a critical cofactor for thrombin-mediated activation of protein C. Activated protein C is best known for its natural anticoagulant and anti-inflammatory properties. Recent evidence has revealed that TM also has protein C- and thrombin-independent physiological function. This review summarizes recent investigations of TM, giving an overview on the TM unique effects on cellular proliferation, adhesion and inflammation, all of which are important steps in atherosclerosis. The current evidence of TM in the pathogenesis of atherosclerosis will be reviewed, and the associations of TM gene polymorphisms with atherosclerosis are presented. Newly emerging data of the TM in mouse atherosclerosis model demonstrates that TM potentially may have therapeutic role in atherosclerosis.
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PMID:The role of thrombomodulin in atherosclerosis: from bench to bedside. 1661 Oct 51

Objective: The present study was designed to identify potential diagnostic markers for acute myocardial infarction (AMI) and determine the significance of immune cell infiltration in this pathology. Methods: Two publicly available gene expression profiles (GSE66360 and GSE48060 datasets) from human AMI and control samples were downloaded from the GEO database. Differentially expressed genes (DEGs) were screened between 80 AMI and 71 control samples. The LASSO regression model and support vector machine recursive feature elimination (SVM-RFE) analysis were performed to identify candidate biomarkers. The area under the receiver operating characteristic curve (AUC) value was obtained and used to evaluate discriminatory ability. The expression level and diagnostic value of the biomarkers in AMI were further validated in the GSE60993 dataset (17 AMI patients and 7 controls). The compositional patterns of the 22 types of immune cell fraction in AMI were estimated based on the merged cohorts using CIBERSORT. Results: A total of 27 genes were identified. The identified DEGs were mainly involved in carbohydrate binding, Kawasaki disease, atherosclerosis, and arteriosclerotic cardiovascular disease. Gene sets related to atherosclerosis signaling, primary immunodeficiency, IL-17, and TNF signaling pathways were differentially activated in AMI compared with the control. IL1R2, IRAK3, and THBD were identified as diagnostic markers of AMI (AUC = 0.877) and validated in the GSE60993 dataset (AUC = 0.941). Immune cell infiltration analysis revealed that IL1R2, IRAK3, and THBD were correlated with M2 macrophages, neutrophils, monocytes, CD4+ resting memory T cells, activated natural killer (NK) cells, and gamma delta T cells. Conclusion: IL1R2, IRAK3, and THBD can be used as diagnostic markers of AMI, and can provide new insights for future studies on the occurrence and the molecular mechanisms of AMI.
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PMID:Predicting Diagnostic Gene Biomarkers Associated With Immune Infiltration in Patients With Acute Myocardial Infarction. 3319 75


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