LAUSR

volume 18 | JuNe 2021 | 387 Furthermore, in a mouse model of SARS-CoV-2 infection, treatment with a BET inhibitor decreased the transcription of genes related to the viral response. “Using a number of omic-based approaches, we identified a therapeutically targetable mechanism, BRD4 activation along with a STAT1-mediated viral response, in which BET inhibition could prevent and recover cardiac dysfunction,” states Mills. Finally, treatment with the commercially available bromodomain 2 (BD2)-selective BET inhibitor apabetalone reduced the cytokine storm-induced diastolic dysfunction and reduced angiotensin converting enzyme 2 levels and viral infection in cardiomyocytes. These data suggest that BD2-selective BET inhibitors are leading candidates for rapid clinical translation for the prevention of cardiac injury in patients with COVID-19. “We believe that BET inhibitors are attractive candidates for many indications in which inflammation could drive cardiac dysfunction, including other viral infections, sepsis and myocarditis,” remarks Mills. “Owing to the lack of effective treatments for many of these diseases, BET inhibitors potentially have huge implications for patient care,” he concludes.