Michael Alexanian’s lab is interested in understanding the genetic and epigenetic mechanisms that govern cell identity in health and disease, with a particular focus on heart disease. In the setting of heart failure, stress induces changes that activate a subset of heart cells, altering their form and function and promoting disease progression. The Alexanian Lab is interested in dissecting the gene-level changes that underlie this effect, in order to design targeted therapies to preserve or restore heart function.
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Alexanian’s work provides deep mechanistic insight into the epigenomic basis of cellular plasticity in heart disease. Most recently, his research revealed the mechanism underlying the beneficial effect of small molecule bromodomain inhibitors in heart failure, demonstrating that rather than affecting cardiomyocytes, the drugs control the activation of fibroblasts, with direct impact on cardiac function.
The Alexanian Lab studies how chromatin receives, processes, and amplifies environmental stress signals that drive changes in cell states leading to human diseases such as heart failure. The team’s long-term goal is to contribute to the understanding of how to target gene regulation in a cell-specific manner to treat heart disease.
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