Why the study?
Sequencing data suggest HCM may involve mechanisms independent of sarcomeric gene mutations, such as interactions among multiple genes and dysregulated expression.
Population
Data on human heart-specific gene expression, miRNA-target, and protein-protein interactions from open databases
Design
Bioinformatic network-based analysis
Authors
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Bioinformatic analysis challenges monogenic HCM model; leaves open validation of polygenic pathways in clinical cohorts.
A network-based bioinformatic approach identified TGFβ-mediated SMAD signaling pathways as potentially contributing to cardiac remodeling in hypertrophic cardiomyopathy.
Osmak et al. (2021) studied this question.
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