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Atrial myopathy, characterized by progressive metabolic, electrical, and structural changes, creates the arrhythmogenic substrate that drives AF. Defining the key drivers of atrial myopathic processes is essential for targeted therapies that can mitigate AF progression. Here we explore how reduced ERBB4 expression contributes to the development of left atrial myopathy.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>\n                    We analyzed the Cleveland Clinic Biobank to compare left atrial\n                    <jats:italic>ERBB4<\/jats:italic>\n                    levels in patients grouped by AF diagnosis. To investigate the impact of reduced ERBB4 levels on atrial tissue substrate, we created mouse models of cardiac-specific\n                    <jats:italic>Erbb4<\/jats:italic>\n                    deficiency using Mlc2a (myosin light chain 2a)-Cre. Comprehensive physiological assessments were performed. Transcriptomic analyses of the left atrium were performed in an\n                    <jats:italic>Erbb4<\/jats:italic>\n                    haploinsufficient mouse model and compared with human atrial datasets. Molecular validation of key dysregulated pathways was performed.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>\n                    We found that left atrial\n                    <jats:italic>ERBB4<\/jats:italic>\n                    levels are reduced in patients with AF. Adult cardiomyocyte-specific\n                    <jats:italic>Erbb4<\/jats:italic>\n                    heterozygous (\n                    <jats:italic>Erbb4<\/jats:italic>\n                    <jats:sup>fl\/+<\/jats:sup>\n                    ;Mlc2a-Cre) mice exhibited prolonged P-wave duration in the absence of ventricular dysfunction. Left atrial transcriptomic analysis in\n                    <jats:italic>Erbb4<\/jats:italic>\n                    haploinsufficient mice showed upregulation of pathways related to fibrosis, apoptosis, and coagulation, and downregulation of pathways related to fatty acid metabolism and mitochondrial function, mirroring changes observed in pressure overload mouse models. A cross-species transcriptomic comparison revealed significant overlap between\n                    <jats:italic>ERBB4<\/jats:italic>\n                    -correlated gene expression and functional pathways in adult human atria and mice with\n                    <jats:italic>Erbb4<\/jats:italic>\n                    haploinsufficiency. Validating the transcriptomic data, protein and functional assays demonstrated increased fibrosis, apoptosis, and oxidative stress in the mutant left atrial tissue.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>\n                    Left atrial\n                    <jats:italic>ERBB4<\/jats:italic>\n                    levels are reduced in AF patients. A mouse model of\n                    <jats:italic>Erbb4<\/jats:italic>\n                    deficiency and human atrial transcriptomic analyses highlight a role for ERBB4 in supporting normal atrial metabolism while protecting against inflammation, apoptosis, and fibrosis.\n                  <\/jats:p>\n                <\/jats:sec>","DOI":"10.64898\/2026.05.26.26354173","type":"posted-content","created":{"date-parts":[[2026,5,28]],"date-time":"2026-05-28T03:55:17Z","timestamp":1779940517000},"source":"Crossref","is-referenced-by-count":0,"title":["ERBB4 deficiency promotes atrial myopathy underlying the atrial fibrillation substrate"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6042-3529","authenticated-orcid":false,"given":"Naoko","family":"Yamaguchi","sequence":"first","affiliation":[{"name":"The Leon H. 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