Plakophilin-2 truncating variants impair cardiac tissue contractility by destabilizing cell-cell junctions and disrupting sarcomere stability and organization.
Plakophilin-2 truncating variants disrupt cardiomyocyte structure and function by destabilizing cell-cell junctions and sarcomeres, revealing a fundamental pathogenic mechanism for cardiomyopathies.
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tvs impair cardiac tissue contractility by destabilizing cell-cell junctions and in turn disrupting sarcomere stability and organization. These findings highlight the interplay between cell-cell adhesions and sarcomeres required for stabilizing cardiomyocyte structure and function and suggest fundamental pathogenic mechanisms that may be shared among different types of cardiomyopathies.
Zhang et al. (Fri,) reported a other. Plakophilin-2 truncating variants impair cardiac tissue contractility by destabilizing cell-cell junctions and disrupting sarcomere stability and organization.