{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,14]],"date-time":"2025-10-14T11:35:48Z","timestamp":1760441748149,"version":"3.40.5"},"reference-count":48,"publisher":"Wiley","license":[{"start":{"date-parts":[[2022,8,2]],"date-time":"2022-08-02T00:00:00Z","timestamp":1659398400000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Disease Markers"],"published-print":{"date-parts":[[2022,8,2]]},"abstract":"<jats:p>Background. Coronary atherosclerotic heart disease (CHD) is a lethal disease with an unstated pathogenic mechanism. Therefore, it is urgent to develop innovative strategies to ameliorate the outcome of CHD patients and explore novel biomarkers connected to the pathogenicity of CHD. Methods. The weighted gene coexpression network analysis (WGCNA) was carried out on a coronary atherosclerosis dataset GSE90074 to determine the crucial modules and hub genes for their prospective relationship to CHD. After the different modules associated with CHD have been identified, the Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enriched pathway analyses were conducted. The protein-protein interaction (PPI) network was thereafter performed for the critical module using STRING and Cytoscape. Results. The yellow module was recognized as the most critical module associated with CHD. The enriched pathways in the yellow module included those related to inflammatory response, positive regulation of extracellular signal-regulated kinase1\/2 (ERK1\/2) cascade, lipid catabolic process, cellular response to oxidative stress, apoptotic pathway, and NF-kappa B pathway. Further CytoHubba analysis revealed the top five hub genes (MMP14, CD28, CaMK4, RGS1, and DDAH1) associated with CHD development. Conclusions. The current study provides the prognosis, novel hub genes, and signaling pathways for treating coronary atherosclerosis. However, their potential biological roles require deeper investigation.<\/jats:p>","DOI":"10.1155\/2022\/6971238","type":"journal-article","created":{"date-parts":[[2022,8,2]],"date-time":"2022-08-02T19:10:04Z","timestamp":1659467404000},"page":"1-13","source":"Crossref","is-referenced-by-count":3,"title":["Weighted Gene Coexpression Network Analysis Identifies Crucial Genes Involved in Coronary Atherosclerotic Heart Disease"],"prefix":"10.1155","volume":"2022","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1016-2455","authenticated-orcid":true,"given":"Jinli","family":"Bao","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Municipal Hospital, Zaozhuang, Shandong 277100, China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","reference":[{"key":"1","doi-asserted-by":"publisher","DOI":"10.1136\/heartjnl-2021-319296"},{"key":"2","doi-asserted-by":"publisher","DOI":"10.3389\/fphar.2020.00195"},{"key":"3","doi-asserted-by":"publisher","DOI":"10.1016\/j.scitotenv.2020.136608"},{"key":"4","doi-asserted-by":"publisher","DOI":"10.1186\/s40359-019-0295-y"},{"key":"5","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.118.039357"},{"key":"6","doi-asserted-by":"publisher","DOI":"10.3389\/fcvm.2020.622236"},{"key":"7","doi-asserted-by":"publisher","DOI":"10.1016\/j.gene.2020.145354"},{"key":"8","doi-asserted-by":"publisher","DOI":"10.1016\/j.atherosclerosis.2021.02.017"},{"key":"9","doi-asserted-by":"publisher","DOI":"10.1038\/s41396-020-0658-7"},{"key":"10","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCGENETICS.109.899443"},{"key":"11","doi-asserted-by":"publisher","DOI":"10.1186\/s12918-017-0420-6"},{"key":"12","doi-asserted-by":"publisher","DOI":"10.1016\/j.cancergen.2020.01.052"},{"key":"13","doi-asserted-by":"publisher","DOI":"10.1111\/jcmm.15432"},{"issue":"1","key":"14","first-page":"1","article-title":"Potential biomarkers of acute myocardial infarction based on weighted gene co-expression network analysis","volume":"18","author":"L. 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