The Bristow Laboratory investigates chronic heart failure, specifically the molecular mechanisms involved in the genesis and progression of pathologic hypertrophy and contractile dysfunction that are hallmarks of this disease. We measure myocardial gene expression in human clinical studies, and we also work with animal and cell models to gain an understanding of how gene expression changes relate to phenotypic changes and/or differences. More recently, based on previous work we did with the human heart ACE2 enzyme, we have added to the area of investigation mechanisms by which the SARS-CoV-2 virus attaches to, enters and damages myocardial cells.
Our studies correlating expression and phenotype have also allowed us to determine some of the genetic basis for the variability in therapeutic responses routinely observed for most classes of drugs, and these observations have been useful in the development of new pharmaceutical and device-based approaches to treat heart failure and other cardiovascular diseases. Over a more than 30 year period we have collected and processed diseased and control human heart samples from transplant and organ donor programs to create what is likely the largest tissue bank of its kind in the world. This tissue bank has proved extremely helpful in generating key hypotheses about important pathophysiological mechanisms, as well as in the discovery of genetic variants important in therapeutic responses.
2020:
2019:
Dose Response of β-Blockers in Adrenergic Receptor Polymorphism Genotypes.
Association of Variants in BAG3 With Cardiomyopathy Outcomes in African American Individuals.
Changing the Research Culture in the United States.
Heart Rate in Preserved Ejection Fraction Heart Failure.
Genetic variation expressed in the brain may impact heart failure.
Myocardial microRNAs associated with reverse remodeling in human heart failure.
2016:
Fine Tuning Adenylyl Cyclase as a (Gene) Therapy for Heart Failure.
2015:
Visual analysis of biological data-knowledge networks.
Cardiovascular drug development: is it dead or just hibernating?