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Pharmacol."],"abstract":"<jats:p><jats:bold>Background:<\/jats:bold> Non-alcoholic fatty liver disease (NAFLD) and atrial fibrillation (AF) are major health burdens, with emerging evidence suggesting NAFLD as a significant risk factor for AF, but the mechanism is remain unclear.<\/jats:p><jats:p><jats:bold>Methods:<\/jats:bold> In this study, we analyzed gene expression data from NAFLD (GSE89632) and AF (GSE75092) datasets from the Gene Expression Omnibus. We identified co-upregulated and co-downregulated genes between NAFLD and AF, assessed diagnostic potential of specific genes, conducted immune infiltration analysis, and performed molecular docking studies with sodium glucose co-transporter 2 inhibitors (SGLT2i).<\/jats:p><jats:p><jats:bold>Results:<\/jats:bold> We identified eight co-upregulated and 31 co-downregulated genes between NAFLD and AF. Genes such as <jats:italic>AMOT<\/jats:italic>, <jats:italic>PDE11A<\/jats:italic>, <jats:italic>TYMS<\/jats:italic>, <jats:italic>TMEM98<\/jats:italic>, and <jats:italic>PTGS2<\/jats:italic> demonstrated substantial diagnostic potential for identifying NAFLD patients at risk of AF. Immune infiltration analysis discovered an elevated presence of CD8 T cells, \u03b3\u03b4 T cells, and M2 macrophages in NAFLD livers, linking systemic inflammation to NAFLD and AF. Additionally, studies have shown that a connection between mitochondrial dysfunction and several hub genes like <jats:italic>DGAT1<\/jats:italic>, <jats:italic>TYMS<\/jats:italic>, and <jats:italic>PTGS2<\/jats:italic>, suggesting that mitochondrial disturbances may underpin the systemic inflammation in NAFLD, which possibly exacerbating AF. Molecular docking studies indicated that empagliflozin's binding affinity with key genes such as <jats:italic>DGAT1<\/jats:italic>, <jats:italic>TYMS<\/jats:italic>, and <jats:italic>PTGS2<\/jats:italic> presents a novel therapeutic avenue for NAFLD-associated AF.<\/jats:p><jats:p><jats:bold>Conclusion:<\/jats:bold> Our study firstly discovered that <jats:italic>AMOT, PDE11A, TYMS, TMEM98<\/jats:italic>, and <jats:italic>PTGS2<\/jats:italic> are associated with NAFLD-related AF and hold strong diagnostic values. Our study also indicates that mitochondrial dysfunction and systemic inflammation may be potential mechanisms bridging NAFLD and AF. Additionally, we identified empagliflozin as a potentially effective therapeutic agent for NAFLD-related AF at the molecular structure level. These novel insights contribute to the further understanding, diagnosis, and intervention of NAFLD-related AF.<\/jats:p>","DOI":"10.3389\/fphar.2024.1360974","type":"journal-article","created":{"date-parts":[[2024,3,14]],"date-time":"2024-03-14T04:52:34Z","timestamp":1710391954000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":10,"title":["Identification of key genes increasing susceptibility to atrial fibrillation in nonalcoholic fatty liver disease and the potential mechanisms: mitochondrial dysfunction and systemic inflammation"],"prefix":"10.3389","volume":"15","author":[{"given":"Baiyin","family":"Zhong","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhonghui","family":"Xie","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jianhong","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xing","family":"Xie","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuankang","family":"Xie","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Binhui","family":"Xie","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chuanbin","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2024,3,14]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"2286","DOI":"10.1002\/hep4.2005","article-title":"Favorable impact of long-term SGLT2 inhibitor for NAFLD complicated by diabetes mellitus: a 5-year follow-up study","volume":"6","author":"Akuta","year":"2022","journal-title":"Hepatol. 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