Mice Deficient in TAZ (Wwtr1) Demonstrate Clinical Features of Late-Onset Fuchs’ Endothelial Corneal Dystrophy

Abstract

There are common phenotypic abnormalities seen between Wwtr1 deficient and FECD-affected patients, suggesting that Wwtr1 deficient mice could function as a murine model of late-onset FECD. Despite the lack of a genetic association between FECD and WWTR1, aberrant WWTR1/TAZ protein subcellular localization and degradation may play critical roles in the pathogenesis of FECD.