Corneal endothelial cell dysfunction: etiologies and management

Abstract

A transparent cornea is essential for the formation of a clear image on the retina. The human cornea is arranged into well-organized layers, and each layer plays a significant role in maintaining the transparency and viability of the tissue. The endothelium has both barrier and pump functions, which are important for the maintenance of corneal clarity. Many etiologies, including Fuchs’ endothelial corneal dystrophy, surgical trauma, and congenital hereditary endothelial dystrophy, lead to endothelial cell dysfunction. The main treatment for corneal decompensation is replacement of the abnormal corneal layers with normal donor tissue. Nowadays, the trend is to perform selective endothelial keratoplasty, including Descemet stripping automated endothelial keratoplasty and Descemet’s membrane endothelial keratoplasty, to manage corneal endothelial dysfunction. This selective approach has several advantages over penetrating keratoplasty, including rapid recovery of visual acuity, less likelihood of graft rejection, and better patient satisfaction. However, the global limitation in the supply of donor corneas is becoming an increasing challenge, necessitating alternatives to reduce this demand. Consequently, in vitro expansion of human corneal endothelial cells is evolving as a sustainable choice. This method is intended to prepare corneal endothelial cells in vitro that can be transferred to the eye. Herein, we describe the etiologies and manifestations of human corneal endothelial cell dysfunction. We also summarize the available options for as well as recent developments in the management of corneal endothelial dysfunction.

Variable Responses to Corneal Grafts: Insights from Immunology and Systems Biology

“…Other components of the immune milieu, including various cytokines and mediator cells, contribute to the decompensation of the corneal endothelium when their balance shifts [42,49]. Corneal edema and bullous keratopathy often signal graft failure, and these conditions are often characterized by dystrophic changes in the Descemet's membrane and stroma that are partially, if not largely, caused by immune responses [50]. Keratocytes within the epithelium and stroma, endothelial cells, and immune cells brought to the cornea through homing mechanisms all contribute to the corneal immune response through cytokine and chemokine secretion, assisted by the expression of various adhesion proteins in the corneal cells [21,24,26,[28][29][30][34][35][36][37].…”

Correlations between corneal biomechanics and specular microscopy in patient with cataract

“…Specular microscopy is a noninvasive method for analyzing the corneal endothelium and facilitates the rapid and correct diagnosis of corneal endotheliopathy affecting the structure and physiology of this corneal layer [ 14 - 17 ].…”

Development of Animal Models for Lens and Corneal Diseases Using N-Methyl-N-Nitrosourea

“…With the rate of cataract surgery growing exponentially, 14 cataract surgery, typically phacoemulsification, is the most common cause of corneal endothelial decompensation. [30][31][32][33][34][35] Corneal endothelium decompensation occurs as a surgical complication in 1 to 2% of cataract surgeries. 30,36,37 Cornea edema after cataract surgery was the predominant indication for penetrating keratoplasty in North America (28.0%) and ranked second in Europe (20.6%), Australia (21.1%), the Middle East (13.6%), Asia (15.5%), and South America (18.6%).…”

“…[30][31][32][33][34][35] Corneal endothelium decompensation occurs as a surgical complication in 1 to 2% of cataract surgeries. 30,36,37 Cornea edema after cataract surgery was the predominant indication for penetrating keratoplasty in North America (28.0%) and ranked second in Europe (20.6%), Australia (21.1%), the Middle East (13.6%), Asia (15.5%), and South America (18.6%). 35 In previous studies, staining for 8-hydroxy-2deoxyguanosine (8-OHdG), a marker of oxidative stress, has revealed that the free radicals produced by phacoemulsification cause damage to the corneal endothelium.…”