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This Viewpoint explores the potential for genetic therapies to treat inherited cardiomyopathies at the intersection of unmet clinical need, patient appetite, and technological advances.
Findings indicate that uORF-mediated repression of TTN is context-dependent and not recapitulated in a disease-relevant model, which highlights the complex regulation of TTN expression and the importance of validating regulatory elements in their endogenous context.
SVIL-associated cardiomyopathy is established as a mechanistically distinct form of HCM and drugs targeting mitochondrial bioenergetics may be a therapeutic strategy in patients with SVIL-associated cardiomyopathy.
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