SLC4A11 and congenital hereditary endothelial dystrophy of cornea: Transcriptomic analysis of corneal endothelium and body composition analysis in Slc4a11<sup>+/+</sup> and Slc4a11<sup>-/-</sup> mice suggest that estrogens play a role in promoting corneal endothelial utilization of lipids via β-oxidation as an alternative energy source in the absence of SLC4A11-mediated NH<sub>3</sub>:H transport function, thereby reducing oxidative stress from glucose and glutamine metabolism.<h4>Conclusions</h4>Male sex is associated with a more severe corneal phenotype in individuals with CHED and a Slc4a11<sup>-/-</sup> mouse model of the disease.