Abstract
Corneal endothelial cells (CECs) are essential for maintenance of corneal transparency.Proliferative potency of human CECs is poor in vivo, so endothelial dysfunction is irreversible.Many studies have showed that CECs are able to proliferate in vitro.However, endothelial to mesenchymal transition (EndMT) will emerge with CECs acquire a myofibroblastic phenotype and lose their specific markers, which hinders the development of corneal regenerative medicine.EndMT participates in corneal disorders, but its process has not been clarified yet.Now, researchers have found that the mechanism of EndMT may include transforming growth factor-β (TGF-β) signaling pathway, fibroblast growth factors (FGFs), and Notch signaling pathway.Therefore, there are several ways to prevent EndMT, such as inhibiting TGF-β signaling pathway, using anti-phosphatidylinositol 3-kinase antibody, small interfering RNA (siRNA) against p120, Leucine-rich repeat-containing G protein-coupled receptor 5 (LGR5) and LGR5 ligand, inhibiting Notch signaling pathway, making connexin43 knockdown, inhibiting matrix metalloproteinase activity and using Asc-2P.This review elaborated the mechanism of EndMT and ways to prevent or reverse it. Key words: Corneal endothelial cells; Endothelial to mesenchymal transition; Mechanics; Inhibition; Reverse
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