Figure 6

Schematic image shows possible pathophysiology of FECD. High sensitivity to TGF-β and activation of TGF-β signaling pathway induce excessive production of ECM components. ECM components form clinically phenotypic features, namely Descemet’s membrane thickening and guttae formation. At the same time, the overload of ECM proteins will form unfolded protein and trigger the UPR, and the cells will undergo apoptosis through the intrinsic pathway. We also showed that TGF-β signaling pathway might be a possible therapeutic target for treatment of FECD.