Endothelial NADPH oxidase 4 protects against angiotensin II‐induced cardiac fibrosis and inflammation

Aims Endothelial activation and inflammatory cell infiltration have important roles in the development of cardiac fibrosis induced by renin–angiotensin system activation. NADPH oxidases (Nox proteins) are expressed in endothelial cells (ECs) and alter their function. Previous studies indicated that Nox2 in ECs contributes to angiotensin II (AngII)‐induced cardiac fibrosis. However, the effects of EC Nox4 on cardiac fibrosis are unknown. Methods and results Transgenic (TG) mice overexpressing endothelial‐restricted Nox4 were studied alongside wild‐type (WT) littermates as controls. At baseline, Nox4 TG mice had significantly enlarged hearts compared with WT, with elongated cardiomyocytes (increased by 18.5%, P