Akiva E. Greenberg

This study models human iron overload cardiomyopathy in vitro using engineered heart tissues, revealing differential effects on cardiomyocytes and fibroblasts and mechanisms of arrhythmogenesis and reduced contractility.

This paper investigates the structural dynamics of the intrinsically disordered troponin-T linker region using single-molecule FRET, molecular dynamics simulations, and functional assays, showing its dynamic behavior and how a mutation affects intermolecular interactions.

This study shows that loss of p300 and CBP in skeletal muscle causes severe contractile dysfunction, but mitochondrial function and cross-bridge cycling are not the primary causes.

This study connects genotype, phenotype, and drug response in dilated cardiomyopathy using molecular mechanism-based computational and experimental approaches for a troponin T mutation.