Activation of CD38 by hypoxia-reoxygenation depletes NAD(P)+ in cardiac endothelial cells and impairs nitric oxide production by endothelial nitric oxide synthase that utilizes NADPH as the reducing substrate (Forstermann and Sessa, 2012), suggesting that CD38 may cause endothelial dysfunction after ischemic injury (Boslett et al., 2018). Here, CD38 is linked to endothelial dysfunction.