Why the study?
A lack of effective therapies targeting arrhythmogenic cardiomyopathy pathophysiology makes management challenging, highlighting a critical need to understand its underlying mechanistic basis.
Population
Patients with arrhythmogenic cardiomyopathy (ACM) and preclinical models (in vitro and in vivo mouse models)
Design
Review
Authors
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May intensify exercise counseling to cut SCD risk in ACM now; leaves open non-desmosomal targets pending larger studies.
Understanding the molecular basis of arrhythmogenic cardiomyopathy, including desmosomal gene variants and altered Wnt/β-catenin signaling, is critical for developing targeted therapies.
Stevens et al. (2020) studied this question.
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