{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T00:22:40Z","timestamp":1792023760400,"version":"4.4.0"},"reference-count":39,"publisher":"Wiley","issue":"24","license":[{"start":{"date-parts":[[2011,12,14]],"date-time":"2011-12-14T00:00:00Z","timestamp":1323820800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2011,12,15]]},"abstract":"<jats:p>\n                    <jats:bold>Non\u2010technical summary\u2002<\/jats:bold>\n                    Diseases, genetic defects, or ionic imbalances can alter the normal electrical activity of cardiac myocytes causing an anomalous heart rhythm, which can degenerate to ventricular fibrillation (VF) and sudden cardiac death. Well\u2010recognized triggers for VF are aberrations of the cardiac action potential, known as early afterdepolarizations (EADs). In this study, combining mathematical modelling and experimental electrophysiology in real\u2010time (dynamic clamp), we investigated the dependence of EADs on the biophysical properties of the L\u2010type Ca\n                    <jats:sup>2+<\/jats:sup>\n                    current (\n                    <jats:italic>I<\/jats:italic>\n                    <jats:sub>Ca,L<\/jats:sub>\n                    ) and identified modifications of\n                    <jats:italic>I<\/jats:italic>\n                    <jats:sub>Ca,L<\/jats:sub>\n                    properties which effectively suppress EAD. We found that minimal changes in the voltage dependence of activation or inactivation of\n                    <jats:italic>I<\/jats:italic>\n                    <jats:sub>Ca,L<\/jats:sub>\n                    can dramatically reduce the occurrence of EADs in cardiac myocytes exposed to different EAD\u2010inducing conditions. This work assigns a critical role to the L\u2010type Ca\n                    <jats:sup>2+<\/jats:sup>\n                    channel biophysical properties for EADs formation and identifies the L\u2010type Ca\n                    <jats:sup>2+<\/jats:sup>\n                    channel as a promising therapeutic target to suppress EADs and their arrhythmogenic effects.\n                  <\/jats:p>","DOI":"10.1113\/jphysiol.2011.219600","type":"journal-article","created":{"date-parts":[[2011,10,25]],"date-time":"2011-10-25T00:41:30Z","timestamp":1319503290000},"page":"6081-6092","source":"Crossref","is-referenced-by-count":57,"title":["Shaping a new Ca\n                    <sup>2+<\/sup>\n                    conductance to suppress early afterdepolarizations in cardiac myocytes"],"prefix":"10.1113","volume":"589","author":[{"given":"Roshni V.","family":"Madhvani","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuanfang","family":"Xie","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antonios","family":"Pantazis","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alan","family":"Garfinkel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhilin","family":"Qu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James 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