Still, whereas human DD and HFpEF present with many different phenotypes and are associated with various comorbidities, inflammation, endothelial dysfunction, and NO-depletion are known and common denominators of HFpEF in humans.43,44 Although our data indicate that NOX1 may be regulated in peripheral monocytes in pro-inflammatory conditions associated with DD and HFpEF in humans, further studies are needed to delineate the precise contribution of NOX1 in macrophages or other inflammatory cells in DD and HFpEF in general and in metabolic heart disease in particular. This evidence concerns the gene NOX1 and dentin dysplasia.