PDF(Pubmed)
Abstract：
Diabetes mellitus, the most prevalent endocrine disorder, not only impacts the retina but also significantly involves the ocular surface. Diabetes contributes to the development of dry eye disease and induces morphological and functional corneal alterations, particularly affecting nerves and epithelial cells. These changes manifest as epithelial defects, reduced sensitivity, and delayed wound healing, collectively encapsulated in the context of diabetic keratopathy. In advanced stages of this condition, the progression to corneal ulcers and scarring further unfolds, eventually leading to corneal opacities. This critical complication hampers vision and carries the potential for irreversible visual loss. The primary objective of this review article is to offer a comprehensive overview of the pathomechanisms underlying diabetic keratopathy. Emphasis is placed on exploring the redox molecular pathways responsible for the aberrant structural changes observed in the cornea and tear film during diabetes. Additionally, we provide insights into the latest experimental findings concerning potential treatments targeting oxidative stress. This endeavor aims to enhance our understanding of the intricate interplay between diabetes and ocular complications, offering valuable perspectives for future therapeutic interventions.
摘要：
糖尿病,最普遍的内分泌紊乱,不仅影响视网膜，而且显著涉及眼表。糖尿病有助于干眼病的发展，并引起形态学和功能性角膜改变，特别影响神经和上皮细胞。这些变化表现为上皮缺陷，灵敏度降低,和延迟的伤口愈合，共同封装在糖尿病性角膜病变的背景下。在这种情况的晚期，角膜溃疡和疤痕的进展进一步展开，最终导致角膜混浊.这种严重的并发症阻碍了视力，并有可能导致不可逆转的视力丧失。本文的主要目的是全面概述糖尿病性角膜病变的病理机制。重点放在探索负责糖尿病期间在角膜和泪膜中观察到的异常结构变化的氧化还原分子途径。此外,我们提供了有关针对氧化应激的潜在治疗方法的最新实验发现的见解。这项工作旨在加强我们对糖尿病和眼部并发症之间复杂相互作用的理解。为未来的治疗干预提供有价值的观点。
