MicroRNA of Epithelial to Mesenchymal Transition in Fuchs’ Endothelial Corneal Dystrophy

Abstract

Aim: a review of miRNA expression connected to epithelial mesenchymal transition studies in Fuchs’ endothelial corneal dystrophy (FECD). Methods: literature search strategy—PubMed central database, using “miRNA” or “microRNA“ and “epithelial mesenchymal transition” or “EMT“ and “Fuchs’ endothelial corneal dystrophy” or “FECD” as keywords. Experimental or clinical studies on humans published in English regarding miRNA profiles of epithelial mesenchymal transition in Fuchs’ endothelial corneal dystrophy published between 2009 and 2022 were included. Conclusion: The publications regarding the miRNA profiles of epithelial mesenchymal transition in Fuchs’ endothelial corneal dystrophy are scarce but provide some valuable information about the potential biomarkers differentiating aging changes from early disease stages characterized by epithelial mesenchymal transition. In the corneal tissue of FECD patients, miRNA-184 seed-region mutation as well as unidirectional downregulation of total miRNA expression led by the miRNA-29 were demonstrated. For early diagnostics the miRNA of epithelial mesenchymal transition in aqueous humor should be analyzed and used as biomarkers.

Absence of the Klotho Function Causes Cornea Degeneration with Specific Features Resembling Fuchs Endothelial Corneal Dystrophy and Bullous Keratopathy

“…For example, a key age-related clinical feature of the cornea is the disruption of the epithelial barrier function, resulting in cornea surface irregularities [36]. Aged corneas also express some characteristics similar to those found in FECD [11]. Thus, the prevalence of DED and its associated visual impairment is widely known to increase significantly with age [32,36].…”

“…With the development of FECD, the accelerated aging mechanisms lead to a loss of endothelial cells [ 10 , 12 ]. However, in the early stage, it is difficult to differentiate FECD pathogenesis from the corneal changes in normal aging [ 11 ]; despite this, FECD is a leading cause of corneal endothelial (CE) degeneration and can result in impaired visual acuity, particularly in women [ 9 , 12 ].…”

“…Endothelial cells are distorted and atrophied during aging, along with an increase in Descemet’s membrane thickness [ 6 ]. One example of age-related endothelial atrophy is the condition of Fuchs endothelial corneal dystrophy (FECD) [ 8 ], a complex age-related genetic disorder [ 9 , 10 ] that begins in the central cornea [ 11 ]. Mature corneal endothelial cells (CECs) do not have the ability to regenerate [ 8 ], but are liable to be damaged by the elevated oxidative stress associated with aging [ 2 , 10 ], leading to accelerated endothelial cell loss [ 8 ], with a subsequent accumulation of excess fluid in the cornea.…”

“…The clinical manifestations of FECD at early stages are hardly distinguished from the corneal changes during normal aging [ 11 ]. Also, due to the complex etiology of FECD, which involves both genetic and environmental factors, there is currently a lack of therapeutic intervention [ 12 ].…”