Key result
Connexin 43 levels and basal ICa,L were decreased in atrial fibrillation subjects compared to sinus rhythm controls, and Cx43 knockdown inhibited calcium channel protein levels and currents.
Why the study?
Atrial fibrillation is linked to conduction disturbances from electrical or structural remodelling, but whether connexin interacts with calcium channels in AF pathogenesis remains unclear.
Does Connexin 43 interact with calcium channels to participate in atrial electrical remodeling in atrial fibrillation?
Does Connexin 43 interact with calcium channels to participate in atrial electrical remodeling in atrial fibrillation?
Connexin 43 regulates L-type and T-type calcium currents through colocalization with calcium channel subunits in atrial myocytes, representing a potential mechanism for atrial electrical remodeling in AF.
Answers are grounded in this paper and cite their sources.
Cx43-calcium channel interaction may contribute to AF remodeling; leaves open therapeutic targeting pending human validation.
Atrial fibrillation (AF) is associated with atrial conduction disturbances caused by electrical and/or structural remodelling. 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‐cell patch clamp showed that protein levels of Cav1.2 and connexin 43 (Cx43) and basal ICa,L were decreased in AF subjects compared to sinus rhythm (SR) controls. In cultured atrium‐derived myocytes (HL‐1 cells), knocking‐down of Cx43 or incubation with 30 mmol/L glycyrrhetinic acid significantly inhibited protein levels of Cav1.2 and Cav3.1 and the current density of ICa,L and ICa,T. Incubation with nifedipine or mibefradil decreased the protein level of Cx43 in HL‐1 cells. Moreover, Cx43 was colocalized with Cav1.2 and Cav3.1 in atrial myocytes. Therefore, Cx43 might regulate the ICa,L and ICa,T through colocalization with calcium channel subunits in atrial myocytes, representing a potential pathogenic mechanism in AF.
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Peng et al. (2021) studied Atrial fibrillation. Connexin 43 knockdown or inhibition vs. Sinus rhythm controls / untreated cells was evaluated on Protein levels of Cav1.2 and Cx43 and basal ICa,L. Connexin 43 levels and basal ICa,L were decreased in atrial fibrillation subjects compared to sinus rhythm controls, and Cx43 knockdown inhibited calcium channel protein levels and currents.
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