NOX2 Is Critical to Endocardial to Mesenchymal Transition and Heart Development.

ABSTRACT: NADPH oxidases (NOX) are a major source of reactive oxygen species (ROS) production in the heart. ROS signaling regulates gene expression, cell proliferation, apoptosis, and migration. However, the role of NOX2 in embryonic heart development remains elusive. We hypothesized that deficiency of Nox2 disrupts endocardial to mesenchymal transition (EndMT) and results in congenital septal and valvular defects. Our data show that 34% of Nox2^-/- neonatal mice had various congenital heart defects (CHDs) including atrial septal defects (ASD), ventricular septal defects (VSD), atrioventricular canal defects (AVCD), and malformation of atrioventricular and aortic valves. Notably, Nox2^-/- embryonic hearts show abnormal development of the endocardial cushion a

SUBMITTER: Moazzen H 

PROVIDER: S-EPMC7320281 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature