{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T16:36:31Z","timestamp":1790872591019,"version":"4.1.0"},"reference-count":36,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2014,5,2]],"date-time":"2014-05-02T00:00:00Z","timestamp":1398988800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100007405","name":"The Danish Heart Foundation","doi-asserted-by":"crossref","award":["12-04-R90-A4017-22721"],"award-info":[{"award-number":["12-04-R90-A4017-22721"]}],"id":[{"id":"10.13039\/100007405","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100007405","name":"The Danish Heart Foundation","doi-asserted-by":"crossref","award":["11-04-R84-A3357-22639"],"award-info":[{"award-number":["11-04-R84-A3357-22639"]}],"id":[{"id":"10.13039\/100007405","id-type":"DOI","asserted-by":"crossref"}]},{"name":"The Danish Agency for Science, Technology and Innovation, Medical Research Council","award":["10-084244"],"award-info":[{"award-number":["10-084244"]}]},{"name":"Novo Nordisk Foundation (KC)"},{"name":"Danish National Research Foundation Centre for Cardiac Arrhythmia"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cardiovasc electrophysiol"],"published-print":{"date-parts":[[2014,8]]},"abstract":"<jats:title>The Role of KChIP2 in Heart Failure<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>\n                      K\n                      <jats:sub>V<\/jats:sub>\n                      4 together with K\n                      <jats:sub>V<\/jats:sub>\n                      Channel\u2010Interacting Protein 2 (KChIP2) mediate the fast recovering transient outward potassium current (\n                      <jats:italic>I<\/jats:italic>\n                      <jats:sub>to,f<\/jats:sub>\n                      ) in the heart. KChIP2 is downregulated in human heart failure (HF), potentially underlying the loss of\n                      <jats:italic>I<\/jats:italic>\n                      <jats:sub>to,f<\/jats:sub>\n                      . We investigated remodeling associated with HF hypothesizing that KChIP2 plays a central role in the modulation of outward K\n                      <jats:sup>+<\/jats:sup>\n                      currents in HF.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and Results<\/jats:title>\n                    <jats:p>\n                      HF was induced by aortic banding in wild\u2010type (WT) and KChIP2 deficient (KChIP2\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                      ) mice, evaluated by echocardiography. Action potentials were measured by floating microelectrodes in intact hearts. Ventricular cardiomyocytes were isolated and whole\u2010cell currents were recorded by patch clamp. Left ventricular action potentials in KChIP2\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                      mice were prolonged in a rate dependent manner, consistent with patch\u2010clamp data showing loss of a fast recovering outward K\n                      <jats:sup>+<\/jats:sup>\n                      current and upregulation of the slow recovering\n                      <jats:italic>I<\/jats:italic>\n                      <jats:sub>to,s<\/jats:sub>\n                      and\n                      <jats:italic>I<\/jats:italic>\n                      <jats:sub>Kur<\/jats:sub>\n                      . HF decreased all outward K\n                      <jats:sup>+<\/jats:sup>\n                      currents in WT mice and did not change the relative contribution of\n                      <jats:italic>I<\/jats:italic>\n                      <jats:sub>to,f<\/jats:sub>\n                      in WT mice. Compared to WT HF, KChIP2\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                      HF had a larger reduction of K\n                      <jats:sup>+<\/jats:sup>\n                      \u2010current density. However, the relative APD prolongation caused by HF was shorter for KChIP2\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                      compared with WT, and the APs of the 2 HF mouse types were indistinguishable.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      <jats:italic>I<\/jats:italic>\n                      <jats:sub>to,f<\/jats:sub>\n                      is just one of many K\n                      <jats:sup>+<\/jats:sup>\n                      currents being downregulated in murine HF. The downregulation of repolarizing currents in HF is accentuated in KChIP2\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                      mice. However, the prolongation of APs associated with HF is less in KChIP2\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                      compared to WT, suggesting other compensatory mechanism(s) in the KChIP2\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                      mouse.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jce.12422","type":"journal-article","created":{"date-parts":[[2014,3,28]],"date-time":"2014-03-28T18:23:05Z","timestamp":1396030985000},"page":"896-904","source":"Crossref","is-referenced-by-count":20,"title":["Loss of K\n                    <sup>+<\/sup>\n                    Currents in Heart Failure Is Accentuated in KChIP2 Deficient Mice"],"prefix":"10.1111","volume":"25","author":[{"given":"S\u00d8REN","family":"GRUBB","sequence":"first","affiliation":[{"name":"The Danish National Research Foundation Centre for Cardiac Arrhythmia Department of Biomedical Sciences Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"TOBIAS","family":"SPEERSCHNEIDER","sequence":"additional","affiliation":[{"name":"The Danish National Research Foundation Centre for Cardiac Arrhythmia Department of Biomedical Sciences Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"DONA","family":"OCCHIPINTI","sequence":"additional","affiliation":[{"name":"The Danish National Research Foundation Centre for Cardiac Arrhythmia Department of Biomedical Sciences Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C\u00c9LINE","family":"FISET","sequence":"additional","affiliation":[{"name":"Faculty of Pharmacy Research Center of the Montreal Heart Institute University of Montreal Montreal Quebec Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S\u00d8REN\u2010PETER","family":"OLESEN","sequence":"additional","affiliation":[{"name":"The Danish National Research Foundation Centre for Cardiac Arrhythmia Department of Biomedical Sciences Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"MORTEN B.","family":"THOMSEN","sequence":"additional","affiliation":[{"name":"The Danish National Research Foundation Centre for Cardiac Arrhythmia Department of Biomedical Sciences Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"KIRSTINE","family":"CALLOE","sequence":"additional","affiliation":[{"name":"The Danish National Research Foundation Centre for Cardiac Arrhythmia Department of Biomedical Sciences Faculty of Health and Medical Sciences University of Copenhagen Copenhagen 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