Abstract
Severe systemic inflammation in COVID-19 patients can lead to dysfunction of multiple organs, including the heart. Using an ex vivo cardiac organoid system, Mills et al discovered that inhibitors of the chromatin reader protein, bromodomain-containing protein 4, protect cardiomyocytes from COVID-associated “cytokine storm”. We briefly review these important findings and highlight the translational significance of the work.
Highlights
Severe systemic inflammation in COVID-19 patients can lead to dysfunction of multiple organs, including the heart
Cardiomyocytes express the receptor for severe acute respiratory syndrome (SARS)-CoV-2, angiotensin-converting enzyme 2 (ACE2), which is upregulated in heart failure[2]
INCB054329 binds to BD1 and BD2 of bromodomain and extra-terminal (BET) proteins, thereby functioning as a competitive inhibitor that displaces the readers from acetyl-histones on chromatin
Summary
Severe systemic inflammation in COVID-19 patients can lead to dysfunction of multiple organs, including the heart. The authors initially employed human pluripotent stem cell-derived cardiac organoids (hCOs) in culture to screen different combinations of cytokines and other factors for effects on contractile force or relaxation.
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