角膜内皮细胞EndMT发生机制的研究进展OA

Corneal endothelial cells(CECs),which form the innermost cellular layer of the cornea,play a pivotal role in sustaining corneal transparency and preserving visual acuity.However,CECs are vulnerable to damage induced by a spectrum of pathological conditions or traumatic injuries.Once the density of CECs declines below a critical threshold,corneal endothelial dysfunction is precipitated,ultimately leading to corneal edema and progressive visual impairment.Penetrating keratoplasty and corneal endothelial transplantation remain the first-line therapeutic strategies for managing advanced corneal endothelial dysfunction.Nevertheless,the global shortage of donor corneas severely limits the accessibility and scalability of these surgical interventions.Consequently,regenerative medicine approaches targeting corneal endothelial repair and regeneration have emerged as a major focus of international research in ophthalmology.A key challenge in the in vitro expansion of CECs is their propensity to undergo endothelial-to-mesenchymal transition(EndMT).EndMT is a process of cellular phenotypic transformation,through which endothelial cells lose their intrinsic functions and acquire the characteristic features of mesenchymal cells.The EndMT significantly impedes the clinical translation of in vitro-cultured CECs for regenerative applications.In this review,the risk factors and related signaling pathways involved in EndMT were summarized,aiming to provide references for the basic research and clinical treatment of relevant diseases.