Cytokinesis, Beta-Blockers, and Congenital Heart Disease

This commentary reviews pivotal findings from a study on the cellular basis of congenital heart disease, particularly tetralogy of Fallot with pulmonary stenosis. It emphasizes the role of cytokinesis failure in cardiomyocytes, leading to binucleation and multinucleation due to incomplete cell division. The article highlights how beta-adrenergic signaling may impair this process and presents evidence from murine and human cardiomyocyte studies linking reduced expression of the Ect2 protein to failed cytokinesis. It proposes beta-blockers like propranolol and alprenolol as potential therapies to enhance Ect2 expression and support complete cytokinesis, offering a future avenue for managing congenital cardiac abnormalities.

This commentary reviews pivotal findings from a study on the cellular basis of congenital heart disease, particularly tetralogy of Fallot with pulmonary stenosis. It emphasizes the role of cytokinesis failure in cardiomyocytes, leading to binucleation and multinucleation due to incomplete cell division. The article highlights how beta-adrenergic signaling may impair this process and presents evidence from murine and human cardiomyocyte studies linking reduced expression of the Ect2 protein to failed cytokinesis. It proposes beta-blockers like propranolol and alprenolol as potential therapies to enhance Ect2 expression and support complete cytokinesis, offering a future avenue for managing congenital cardiac abnormalities.