The role of NOX4 in cardiac pressure overload is somewhat unclear, with one study reporting protection by the cardiomyocyte-specific deletion of Nox4, while another study found that the deletion of Nox4 in cardiomyocytes or endothelial cells exacerbated pressure overload-induced cardiac hypertrophy, dysfunction, and fibrosis [99,100]. Here, NOX4 is linked to cardiac hypertrophy.