Authors: Li Weina, Yang Lingling, Xie Lixin
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In recent years, with the increasing incidence of diabetes, diabetic keratopathy has gradually attracted more attention from clinicians.Diabetic keratopathy is mainly manifested as delayed corneal epithelial healing, corneal edema, decreased corneal sensitivity, and neurotrophic corneal ulcer.There are many mechanisms of diabetic keratopathy, including the abnormal accumulation of metabolites, an inflammatory reaction, oxidative stress, the lack of neurotrophic factors, corneal limbal stem cell abnormalities, etc.At present, most of the research on diabetic keratopathy at home and abroad has mainly focused on epithelial damage repair and changes in nerve function, and the pathological mechanism is mainly inflammatory response and apoptosis.Nuclear factor kappa B(NF-κB) is an important transcription regulatory factor, and is involved in regulating the expression of inflammatory factors, chemokines, cell adhesion molecules, apoptosis-related genes, growth factors, and other target genes.Studies have reported that chronic inflammation and epithelial cell apoptosis of the diabetic corneal epithelium are involved in the regulation of the NF-κB signaling pathway, which is also involved in the regulation of diabetic peripheral neuropathy, and diabetic corneal neuropathy belongs to the category of diabetic peripheral neuropathy.The NF-κB signaling pathway is closely related to the occurrence and development of diabetic keratopathy, and this article summarizes its mechanism.