Stuart G. Campbell

This paper uses simulations to show that concentric and eccentric cardiac growth are regulated by ATP homeostasis and titin-based stress, respectively, and can model growth patterns from both genetic and clinical causes.

This study shows that desmoplakin loss causes PKC-dependent sarcomere shortening and contractile dysfunction in cardiomyocytes, leading to heart failure.

The paper develops a signaling network model to investigate genotype-to-phenotype mechanisms in familial cardiomyopathy, showing it can predict experimental outcomes and suggest therapeutic strategies.