Review highlights neuropathy and gene expression in diabetic keratopathy, suggesting pathogenesis insights for treatment.
Diabetic keratopathy (DK) is an ocular complication of diabetes mellitus (DM). Driven by DM‑induced chronic hyperglycemia and its associated metabolic changes, DK is characterized by progressive damage to the corneal epithelium, nerves, stroma and endothelium, manifesting as corneal epitheliopathy, neuropathy, stromal lesions and endotheliopathy. Nuclear proteins (NPs) play essential roles in the regulation of gene expression and physiological activities in the nucleus, and have been implicated in the occurrence and development DM and its complications. The present review provides an overview of DK and highlights the role of core NPs in its pathogenesis, including peroxisome proliferator‑activated receptors, high‑mobility group box 1, enhancer of zeste homolog, phosphatase and tensin homolog and sirtuins. The review underscores that the roles of these NPs in DK remain incompletely understood and highlights the need for further mechanistic studies and clinical trials to advance DK management. Therefore, it is suggested that future research should focus on elucidating the molecular mechanisms of NPs in DK, and developing novel detection techniques and treatment strategies to provide more effective outcomes for patients with DK.
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Xu et al. (2025) studied this question.
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