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Epicardial adipose tissue (EAT), the cardiac visceral fat depot, has been implicated in AF pathogenesis, but the cellular, molecular, and immune features underlying EAT\u2010mediated AF remain elusive.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p xml:lang=\"en\">We combined population\u2010based analysis, Mendelian randomization, single\u2010nucleus RNA sequencing, and biomarker validation. The visceral adipose tissue\u2013AF association was examined in the National Health and Nutrition Examination Survey, genetic evidence was evaluated using Mendelian randomization based on UKB (UK Biobank), EAT was profiled in patients with coronary artery disease (6 with AF, 3 without), and key circulating signals were evaluated in the Fuwai Hospital cohort and UKB.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Higher visceral adipose tissue was associated with increased AF risk in National Health and Nutrition Examination Survey, and Mendelian randomization provided genetic evidence consistent with a potential causal contribution of visceral adipose tissue to AF. Single\u2010nucleus RNA sequencing showed extensive EAT remodeling in patients with coronary artery disease and AF, including impaired neuroprotective and myelin\u2010maintenance programs, metabolic imbalance, profibrotic activation, and a chronic inflammatory milieu with immunoglobulin G\u2013related humoral immune activation. Drug2cell prioritized candidate drug\u2013cell associations across specific EAT cell populations, and summary data\u2013based Mendelian randomization prioritized\n                      <jats:italic toggle=\"no\">PTPRN2<\/jats:italic>\n                      as a putative AF susceptibility gene. Higher plasma interleukin\u201017 levels were associated with postoperative AF in the Fuwai Hospital cohort, whereas circulating interleukin\u201017C and interleukin\u201017D were independently associated with incident AF in the UKB.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">We constructed the first single\u2010nucleus transcriptomic atlas of human AF\u2010related EAT and identified potential mechanisms linking EAT remodeling to arrhythmogenesis. Elevated plasma interleukin\u201017 may serve as a predictive biomarker for AF.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.126.049221","type":"journal-article","created":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T11:16:52Z","timestamp":1787829412000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["Single\u2010Nucleus and Multiomics Profiling of Epicardial Adipose Tissue in Atrial Fibrillation Reveals Novel Mechanisms and Translational Biomarkers"],"prefix":"10.1161","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0009-0008-9714-3548","authenticated-orcid":false,"given":"Shengkang","family":"Huang","sequence":"first","affiliation":[{"name":"Chinese Academy of Medical Sciences and Peking Union Medical College","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ziang","family":"Yang","sequence":"additional","affiliation":[{"name":"Chinese 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