JUN and atrial fibrillation: Therefore, combining with the network pharmacology, GEO differential expression and in vivo experiments, we hypothesize that Que can medicate some key targets such as IL-6, VEGFA, JUN, MMP9, EGFR, CCND1 and other key signaling pathways such as MAPK pathway, lipid and atherosclerosis, AGE-RAGE pathway in diabetic complications and IL-17 pathway, through which Que can inhibit inflammatory expression, oxidative stress, myocardial fibrosis and alleviate AF-induced atrial remodeling and injury.