Daniel Bernstein

This study investigates factors influencing HCM phenotype penetrance by comparing MYH7 mutations in isogenic hiPSC-CMs and shows that beta-adrenergic stimulation and gene dosage affect disease expression.

This study shows that β2-adrenergic receptor signaling is cardioprotective in acute oxidative stress but cardiotoxic in chronic stress, with implications for β-blocker use in cardiovascular disease.

The paper identifies a conserved postprandial metabolite, pTOS, that links nutrient intake to energy balance through a gut-brain pathway in pythons and mice, with potential relevance to humans.

This study uses cryo-ET to show that MYH7 P710R mutations disrupt thick filament organization in HCM cardiomyocytes, leading to sarcomeric disarray and ribosome infiltration.

This study uses AI to show that genome sequencing can predict adverse outcomes after congenital heart defect surgery by identifying damaging genotypes in specific genes.

This study shows that YAP overactivation in HCM mutant cardiomyocytes drives hypertrophy via CCN2 secretion and TGFβ uptake.

The paper examines how genetic, demographic, and clinical factors interact to influence neurodevelopmental outcomes in children with single ventricle heart disease.

This study investigates the effects of the MYH7 G256E mutation on myosin function across multiple scales, finding increased hypercontractility and mitochondrial respiration.

The paper shows that coronary endothelial cells in mouse and human hearts initially show lineage-specific transcriptional differences but later become influenced by location, with adult cells becoming more homogeneous.

This study shows that overexpressing Dach1 in endothelial cells extends coronary arteries and improves heart function after myocardial infarction in mice.

The paper identifies mosaic mutations in blood and cardiac tissue from CHD patients, finding 1% of cases have detectable mosaic variants that may contribute to congenital heart disease.