Exploring corneal endothelial cell dynamics: structure, functions and therapeutic approaches.

The human cornea is a transparent avascular structure that is crucial for transmitting light to the retina. The innermost layer of the cornea is the corneal endothelium, which is located distal to Descemet's membrane, that connects it to the corneal stroma and is responsible for maintaining corneal clarity via barrier and pump functions. Loss of endothelial transparency significantly impairs vision, and the conditions responsible for disrupting transparency include endothelial dysfunction. This review focuses on the treatment of corneal endothelial pathophysiology. The shape of CECs is maintained by the actin filaments, which are located apically as a thick band. Cadherin forms the junctional complex at the apical cell junctions, which further extends up to the basolateral borders of the cells. The ability of the cornea to transmit light depends on the deturgescence of the connective tissue stroma, which is regulated by an active fluid transport system connected to the corneal endothelium. The disruption of the ability of CECs to regulate visual clarity and corneal hydration either indirectly affects the contraction of actomyosin or directly threatens the integrity of barrier function because cell loss leads to corneal edema, epispodic ocular pain, blurred vision or blistering of the corneal endothelium. Once damaged, the corneal endothelium does not regenerate in humans. With the advancement of modern surgical techniques, endothelial corneal dystrophies have become treatable. While pharmacological treatments and emerging therapies are important, surgical approaches remain the cornerstone of treatment. Research into gene therapy, stem cells, and tissue engineering may further transform the management of endothelial corneal dystrophies in the future.