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In the present study, we hypothesized that connexin might interact with the calcium channel through forming a protein complex and, then, participates in the pathogenesis of AF. Western blot and whole\u2010cell patch clamp showed that protein levels of Cav1.2 and connexin 43 (Cx43) and basal <jats:italic>I<jats:sub>Ca<\/jats:sub><\/jats:italic><jats:sub>,<\/jats:sub><jats:italic><jats:sub>L<\/jats:sub><\/jats:italic> were decreased in AF subjects compared to sinus rhythm (SR) controls. In cultured atrium\u2010derived myocytes (HL\u20101 cells), knocking\u2010down of Cx43 or incubation with 30\u00a0mmol\/L glycyrrhetinic acid significantly inhibited protein levels of Cav1.2 and Cav3.1 and the current density of <jats:italic>I<jats:sub>Ca<\/jats:sub><\/jats:italic><jats:sub>,<\/jats:sub><jats:italic><jats:sub>L<\/jats:sub><\/jats:italic> and <jats:italic>I<jats:sub>Ca<\/jats:sub><\/jats:italic><jats:sub>,<\/jats:sub><jats:italic><jats:sub>T<\/jats:sub><\/jats:italic>. Incubation with nifedipine or mibefradil decreased the protein level of Cx43 in HL\u20101 cells. Moreover, Cx43 was colocalized with Cav1.2 and Cav3.1 in atrial myocytes. Therefore, Cx43\u00a0might regulate the <jats:italic>I<jats:sub>Ca<\/jats:sub><\/jats:italic><jats:sub>,<\/jats:sub><jats:italic><jats:sub>L<\/jats:sub><\/jats:italic> and <jats:italic>I<jats:sub>Ca<\/jats:sub><\/jats:italic><jats:sub>,<\/jats:sub><jats:italic><jats:sub>T<\/jats:sub><\/jats:italic> through colocalization with calcium channel subunits in atrial myocytes, representing a potential pathogenic mechanism in AF.<\/jats:p>","DOI":"10.1111\/1440-1681.13580","type":"journal-article","created":{"date-parts":[[2021,8,26]],"date-time":"2021-08-26T17:12:56Z","timestamp":1629997976000},"page":"25-34","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Connexin 43 participates in atrial electrical remodelling through colocalization with calcium channels in atrial 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