Alterations in adhesion junction precede gap junction remodelling during the development of heart failure in cardiomyopathic hamsters (Q28241353)

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Tadamitsu Nakashima

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Hiroki Takanari

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Masafumi Yano

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Genzou Takemura

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Haruo Honjo

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Itsuo Kodama

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Yoichi Mizukami

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Masunori Matsuzaki

Primary prevention of sudden cardiac death in idiopathic dilated cardiomyopathy: the Cardiomyopathy Trial (CAT).

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language of work or name

English

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publication date

1 October 2011

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published in

Cardiovascular Research

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volume

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issue

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page(s)

95-105

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cites work

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Effects of the gap junction uncoupler palmitoleic acid on the activation and repolarization wavefronts in isolated rabbit hearts

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Downregulation of immunodetectable connexin43 and decreased gap junction size in the pathogenesis of chronic hibernation in the human left ventricle

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Electrophysiological effects of remodeling cardiac gap junctions and cell size: experimental and model studies of normal cardiac growth

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Gap junction alterations in human cardiac disease.

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Altered expression of connexin43 contributes to the arrhythmogenic substrate during the development of heart failure in cardiomyopathic hamster

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Dynamics of early contact formation in cultured adult rat cardiomyocytes studied by N-cadherin fused to green fluorescent protein

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Microtubule plus-end-tracking proteins target gap junctions directly from the cell interior to adherens junctions

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Induced deletion of the N-cadherin gene in the heart leads to dissolution of the intercalated disc structure

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Ultrastructural evidence of intercalated disc remodelling in arrhythmogenic right ventricular cardiomyopathy: an electron microscopy investigation on endomyocardial biopsies

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Slow conduction and enhanced anisotropy increase the propensity for ventricular tachyarrhythmias in adult mice with induced deletion of connexin43.

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Dissociated spatial patterning of gap junctions and cell adhesion junctions during postnatal differentiation of ventricular myocardium

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Connexin43 remodeling caused by inhibition of plakophilin-2 expression in cardiac cells

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Suppression of canonical Wnt/beta-catenin signaling by nuclear plakoglobin recapitulates phenotype of arrhythmogenic right ventricular cardiomyopathy

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Cardiac-Specific Loss of N-Cadherin Leads to Alteration in Connexins With Conduction Slowing and Arrhythmogenesis

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