The corneal endothelium is a monolayer lining the back of the cornea and is responsible for maintaining corneal transparency. Human corneal endothelial cells (CECs) have limited proliferative and regenerative capacities because they are arrested in the G1 phase of the cell cycle. Due to the low regenerative capacity and degeneration over time, loss of CECs in the adult human eye is compensated by size expansion of the remaining cells. For healthy adults aged 20–39 years, the average CEC density is around 3,000 cells/mm2, which declines by 0.3% annually1. To preserve corneal transparency, endothelial cell density must remain above a critical threshold, usually 400-500 cells/mm2. Loss or dysfunction of CECs, such as in Fuchs’ endothelial corneal dystrophy (FECD) and pseudophakic bullous keratopathy (PBK), leads to endothelial decompensation, corneal oedema and eventually loss of vision. FECD has a global estimated prevalence of 4-9% in those aged over 50 years old and PBK occurs in 1-2% of patients receiving cataract surgeries. In New Zealand, corneal endothelial diseases, especially FECD, have become more prevalent in recent years2. Therefore, approaches to revitalising or replacing the corneal endothelium are important to improving eye health outcomes. Currently, most of the approaches for corneal endothelial regeneration which have been studied or are under development include surgical treatment, cell therapies, acellular graft substitutes, pharmacological and genetic modulation (Fig 1).
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