NOX1 and dentin dysplasia: Interestingly, indirect inhibition of NOX1 was recently suggested as a therapeutic strategy in the context of aging-related cardiac remodelling and HFpEF.46 This proposition was based on beneficial effects seen in aged mice deficient for G protein-coupled oestrogen receptor (GPER), a molecule that has previously been shown to act as a constitutive activator of NOX1.47 However, to translate these and our findings to human DD and HFpEF, further studies are needed to identify the roles of NOX1 and to also explore NOX1 up- and downstream signalling in different cell types in human disease.