EP News: Basic and Translational

  • Nipavan Chiamvimonvat
    Address reprint requests and correspondence: Dr Nipavan Chiamvimonvat, Department of Internal Medicine and Pharmacology, GBSF 6315, 451 Health Science Dr, University of California, Davis, Davis, CA 95616.
    Department of Internal Medicine and Pharmacology, University of California, Davis, Davis, California
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      Muscle-specific mitsugumin 53 (MG53) is a muscle-specific tripartite motif family member in the heart and participates in membrane repair by recruiting vesicles to the site of injury. Liu et al (Circulation February 14, 2019;, PMID 30760025) investigated the functional roles of cardiac MG53 in the regulation of KChIP2 (a K+ channel interacting protein), transient outward K+ current (Ito,f), and the arrhythmogenic potential in cardiac hypertrophy using genetic ablation of MG53 in a mouse model. KChIP2 and Ito,f density are downregulated in hearts from MG53-knockout mice. MG53 knockout enhances Ito,f remodeling and action potential duration prolongation and increases susceptibility to ventricular arrhythmia in cardiac hypertrophy. Mechanistically, MG53 regulates NF-κB activity by interacting with TAK1 and IκBα and subsequently the expression of the KChIP2 gene. Specifically, MG53 overexpression decreases whereas MG53 knockdown increases NF-κB enrichment at the 5′ regulatory region of the KChIP2 gene. The authors conclude that MG53 is a novel regulator of KChIP2 and Ito,f by modulating NF-κB activity and plays an important role in electrophysiological remodeling in cardiac hypertrophy.
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