{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T14:41:15Z","timestamp":1782916875946,"version":"3.54.5"},"reference-count":48,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2016,8,31]],"date-time":"2016-08-31T00:00:00Z","timestamp":1472601600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Wilhelm-Roux-Program","award":["FKZ 19\/32"],"award-info":[{"award-number":["FKZ 19\/32"]}]},{"name":"Medical Faculty of the Martin-Luther-University Halle-Wittenberg"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Acta Physiologica"],"published-print":{"date-parts":[[2017,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Aim<\/jats:title><jats:p>Several genetically modified mice models were studied so far to investigate the role of cardiac calsequestrin (CSQ2) for the contractile function of the ventricle and for the occurrence of ventricular tachycardia. Using a CSQ2 knockout mouse, we wanted to study also the atrial function of CSQ2.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>The influence of CSQ2 on atrial function and, for comparison, ventricular function was studied in isolated cardiac preparations and by echocardiography as well as electrocardiography in mice with deletion of CSQ2.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Using deletion of exon 1, we have successfully generated a constitutive knockout mouse of the calsequestrin 2 gene (CSQ2<jats:sup>\u2212\/\u2212<\/jats:sup>). CSQ2 protein was absent in the heart (atrium, ventricle), but also in oesophagus and skeletal muscle of homozygous knockout mice. In 6\u2010month\u2010old CSQ2<jats:sup>\u2212\/\u2212<\/jats:sup> mice, relative left atrial weight was increased, whereas relative heart weight was unchanged. The staircase phenomena in paced left atrial preparations on force of contraction and the post\u2010rest potentiation were different between wild type and CSQ2<jats:sup>\u2212\/\u2212<\/jats:sup> indicative for a decreased sarcoplasmic Ca<jats:sup>2+<\/jats:sup> load and supporting an important role of CSQ2 also in the atrium. The incidence of arrhythmias was increased in CSQ2<jats:sup>\u2212\/\u2212<\/jats:sup>. In 2\u2010year\u2010old CSQ2<jats:sup>\u2212\/\u2212<\/jats:sup> mice, cardiac hypertrophy and heart failure were noted possibly as a result of chronically increased cytosolic Ca<jats:sup>2+<\/jats:sup> levels.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>These data suggest a functional role of CSQ2 not only in the ventricle but also in the atrium of mammalian hearts. Loss of CSQ2 function can cause not only arrhythmias, but also cardiac hypertrophy and heart failure.<\/jats:p><\/jats:sec>","DOI":"10.1111\/apha.12766","type":"journal-article","created":{"date-parts":[[2016,8,3]],"date-time":"2016-08-03T12:07:31Z","timestamp":1470226051000},"page":"671-684","source":"Crossref","is-referenced-by-count":22,"title":["Evidence for a functional role of calsequestrin 2 in mouse atrium"],"prefix":"10.1111","volume":"219","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6986-485X","authenticated-orcid":false,"given":"U.","family":"Gergs","sequence":"first","affiliation":[{"name":"Institut f\u00fcr Pharmakologie und Toxikologie Medizinische Fakult\u00e4t Martin\u2010Luther\u2010Universit\u00e4t Halle\u2010Wittenberg Halle\/Saale Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C. 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