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; https://doi.org/10.1161/CIRCULATIONAHA.118.029413, 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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Publication history
Published online: March 22, 2019
