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• W2078261885 startingPage "4" @default.
• W2078261885 abstract "Gap junctions provide direct cytoplasmic continuity between cells forming a low resistivity barrier to electrical propagation. As such, aberrant regulation of these low resistive conduits has been blamed for electrical conduction disorders in diseased myocardium. While there is a plethora of evidence that abnormalities in gap junctional communication underlie many forms of ventricular arrhythmias, the role of gap junctions in atrial conduction disorders has been less well studied. The atria are the most heterogeneous cardiac structures in terms of the gap junction proteins, connexins (Cx), which are present. Cx40 is the primary, or most abundant, gap junction protein in atria although Cx43 is also abundantly expressed. Cx45 is also expressed in atria, although at low levels. This heterogeneity in connexins leads to a complexity that makes understanding the role of cell coupling in conduction disorders and arrhythmogenesis difficult. In this review we focus on what is known about atrial connexins and their role in atrial fibrillation but also on the challenges presented in understanding the complex interplay between the individual connexin isoforms." @default.
• W2078261885 created "2016-06-24" @default.
• W2078261885 creator A5000705640 @default.
• W2078261885 creator A5083425390 @default.
• W2078261885 date "2008-01-01" @default.
• W2078261885 modified "2023-10-16" @default.
• W2078261885 title "Is there a role for remodeled connexins in AF? No simple answers" @default.
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• W2078261885 doi "https://doi.org/10.1016/j.yjmcc.2007.08.016" @default.
• W2078261885 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2243184" @default.
• W2078261885 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17935733" @default.
• W2078261885 hasPublicationYear "2008" @default.
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