{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T02:48:29Z","timestamp":1791600509015,"version":"4.3.4"},"reference-count":86,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2023,8,4]]},"abstract":"<jats:sec>\n            <jats:title>Background:<\/jats:title>\n            <jats:p>\n              <jats:italic>ZFHX3<\/jats:italic>\n              (zinc finger homeobox 3), a gene that encodes a large transcription factor, is at the second-most significantly associated locus with atrial fibrillation (AF), but its function in the heart is unknown. This study aims to identify causative genetic variation related to AF at the\n              <jats:italic>ZFHX3<\/jats:italic>\n              locus and examine the impact of\n              <jats:italic>Zfhx3<\/jats:italic>\n              loss on cardiac function in mice.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods:<\/jats:title>\n            <jats:p>\n              CRISPR-Cas9 genome editing, chromatin immunoprecipitation, and luciferase assays in pluripotent stem cell\u2013derived cardiomyocytes were used to identify causative genetic variation related to AF at the\n              <jats:italic>ZFHX3<\/jats:italic>\n              locus. Cardiac function was assessed by echocardiography, magnetic resonance imaging, electrophysiology studies, calcium imaging, and RNA sequencing in mice with heterozygous and homozygous cardiomyocyte-restricted\n              <jats:italic>Zfhx3<\/jats:italic>\n              loss (\n              <jats:italic>Zfhx3<\/jats:italic>\n              Het and knockout, respectively). Human cardiac single-nucleus ATAC (assay for transposase-accessible chromatin)-sequencing data was analyzed to determine which genes in atrial cardiomyocytes are directly regulated by\n              <jats:italic>ZFHX3<\/jats:italic>\n              .\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results:<\/jats:title>\n            <jats:p>\n              We found single-nucleotide polymorphism (SNP) rs12931021 modulates an enhancer regulating\n              <jats:italic>ZFHX3<\/jats:italic>\n              expression, and the AF risk allele is associated with decreased\n              <jats:italic>ZFHX3<\/jats:italic>\n              transcription. We observed a gene-dose response in AF susceptibility with Zfhx3 knockout mice having higher incidence, frequency, and burden of AF than\n              <jats:italic>Zfhx3<\/jats:italic>\n              Het and wild-type mice, with alterations in conduction velocity, atrial action potential duration, calcium handling and the development of atrial enlargement and thrombus, and dilated cardiomyopathy.\n              <jats:italic>Zfhx3<\/jats:italic>\n              loss results in atrial-specific differential effects on genes and signaling pathways involved in cardiac pathophysiology and AF.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions:<\/jats:title>\n            <jats:p>\n              Our findings implicate\n              <jats:italic>ZFHX3<\/jats:italic>\n              as the causative gene at the 16q22 locus for AF, and cardiac abnormalities caused by loss of cardiac\n              <jats:italic>Zfhx3<\/jats:italic>\n              are due to atrial-specific dysregulation of pathways involved in AF susceptibility. Together, these data reveal a novel and important role for\n              <jats:italic>Zfhx3<\/jats:italic>\n              in the control of cardiac genes and signaling pathways essential for normal atrial function.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circresaha.123.323029","type":"journal-article","created":{"date-parts":[[2023,7,14]],"date-time":"2023-07-14T09:00:20Z","timestamp":1689325220000},"page":"313-329","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":48,"title":["Loss of the Atrial Fibrillation-Related Gene,\n            <i>Zfhx3<\/i>\n            , Results in Atrial Dilation and Arrhythmias"],"prefix":"10.1161","volume":"133","author":[{"given":"Heather S.","family":"Jameson","sequence":"first","affiliation":[{"name":"Cardiovascular Research Center (H.S.J., A.H., M.C.H., L.X., J.Y., A.B., E.R., A.W.H., W.J.H., S.C., M.B., E.S., J.A.M., R.W.M., P.T.E.), Massachusetts General Hospital, 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