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However, whether inflammatory signaling is causally linked to AF pathogenesis in obesity remains elusive. We recently demonstrated that the constitutive activation of the \u2018NACHT, LRR, and PYD Domains-containing Protein 3\u2019 (NLRP3) inflammasome promotes AF susceptibility. In this study, we hypothesized that the NLRP3 inflammasome is a key driver of obesity-induced AF.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>Western blotting was performed to determine the level of NLRP3 inflammasome activation in atrial tissues of obese patients, sheep, and diet-induced obese (DIO) mice. The increased body weight in patients, sheep, and mice was associated with enhanced NLRP3-inflammasome activation. To determine whether NLRP3 contributes to the obesity-induced atrial arrhythmogenesis, wild-type (WT) and NLRP3 homozygous knockout (NLRP3\u2212\/\u2212) mice were subjected to high-fat-diet (HFD) or normal chow (NC) for 10\u2009weeks. Relative to NC-fed WT mice, HFD-fed WT mice were more susceptible to pacing-induced AF with longer AF duration. In contrast, HFD-fed NLRP3\u2212\/\u2212 mice were resistant to pacing-induced AF. Optical mapping in DIO mice revealed an arrhythmogenic substrate characterized by abbreviated refractoriness and action potential duration (APD), two key determinants of reentry-promoting electrical remodeling. Upregulation of ultra-rapid delayed-rectifier K+-channel (Kv1.5) contributed to the shortening of atrial refractoriness. Increased profibrotic signaling and fibrosis along with abnormal Ca2+ release from sarcoplasmic reticulum (SR) accompanied atrial arrhythmogenesis in DIO mice. Conversely, genetic ablation of Nlrp3 (NLRP3\u2212\/\u2212) in HFD-fed mice prevented the increases in Kv1.5 and the evolution of electrical remodeling, the upregulation of profibrotic genes, and abnormal SR Ca2+ release in DIO mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>These results demonstrate that the atrial NLRP3 inflammasome is a key driver of obesity-induced atrial arrhythmogenesis and establishes a mechanistic link between obesity-induced AF and NLRP3-inflammasome activation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/cvr\/cvab024","type":"journal-article","created":{"date-parts":[[2021,1,18]],"date-time":"2021-01-18T23:19:06Z","timestamp":1611011946000},"page":"1746-1759","source":"Crossref","is-referenced-by-count":148,"title":["NLRP3 inflammasome is a key driver of obesity-induced atrial arrhythmias"],"prefix":"10.1093","volume":"117","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2781-0508","authenticated-orcid":false,"given":"Larry","family":"Scott Jr","sequence":"first","affiliation":[{"name":"Department of Molecular Physiology and Biophysics, Baylor College of Medicine , Houston, TX,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anke C","family":"Fender","sequence":"additional","affiliation":[{"name":"Institute of Pharmacology, West German Heart and Vascular Center, University Duisburg-Essen , Essen,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arnela","family":"Saljic","sequence":"additional","affiliation":[{"name":"Laboratory of Cardiac Physiology, Department of Biomedical Sciences, University of Copenhagen , Copenhagen,","place":["Denmark"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luge","family":"Li","sequence":"additional","affiliation":[{"name":"Section of 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