Abstract
Cellular and transgenic animal models with mutant desmosomal genes may help to elucidate the cascade of cellular and molecular events involved in arrhythmogenic cardiomyopathy phenotype development and the clinical relevance of different desmosomal gene variants, either isolated or together. Knowledge of the mechanisms leading from the mutant protein to the clinical phenotype, and the search for genetic or environmental factors that influence the expression of these defective proteins, will allow identification of potential molecular targets for therapeutic intervention to stop disease onset and progression.
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