铁离子在维持角膜细胞正常代谢、DNA合成和修复等生理活动中发挥关键作用，但过量的铁离子可能引发铁稳态失衡继而导致细胞毒性损伤和死亡。圆锥角膜是最常见的扩张性角膜疾病，其典型的Fleischer环是铁稳态失衡的直接证据。圆锥角膜与铁代谢相关的前期研究显示，铁稳态失衡有可能是诱发圆锥角膜发生和发展的潜在致病机制。文章总结了人体及角膜中正常的铁代谢循环以及圆锥角膜铁稳态失衡的证据，并从维持铁稳态角度出发探索可能的治疗策略，为扩张性眼病治疗提供新的思路。

Iron ions are essential for normal metabolism, DNA synthesis, and cellular repair in corneal cells. Nevertheless, an excess of these ions can disrupt iron homeostasis, leading to cellular toxicity, damage, and death. Keratoconus, the most prevalent ectatic corneal disorder, is often marked by the Fleischer ring, which indicates an imbalance in iron homeostasis. A review of early studies on keratoconus and iron metabolism suggests that this imbalance may be a potential pathogenic mechanism contributing to the onset and progression of the disease. This article aims to provide a comprehensive overview of normal iron metabolism in the human body and cornea, highlighting the evidence of iron homeostasis imbalance in keratoconus. It also explores potential therapeutic strategies focused on maintaining iron homeostasis, thereby offering novel insights into the treatment of ectatic eye diseases. 

Meibomian gland dysfunction (MGD) manifests through two main clinical presentations, characterized by the meibomian gland (MG) ductal obstruction or acinar dropout. While previous research has predominantly associated MGD pathogenesis with hyperkeratinization-related MG ductal obstruction and subsequent acinar atrophy, recent cases have shown significant functional acinar loss in the absence of apparent ductal keratinization or blockage. The deterioration of either MG obstruction or dropout exacerbates the condition of the other, suggesting an independent yet interconnected relationship that perpetuates the vicious cycle of MGD. Understanding the distinct pathological features of MG obstruction and dropout is crucial for delineating their etiology and identifying targeted therapeutic strategies. This review explores the nuanced interrelations of MG obstruction and dropout, elucidating potential pathological mechanisms to establish a foundation for early MGD diagnosis and intervention.

Meibomian gland dysfunction (MGD) manifests through two main clinical presentations, characterized by the meibomian gland (MG) ductal obstruction or acinar dropout. While previous research has predominantly associated MGD pathogenesis with hyperkeratinization-related MG ductal obstruction and subsequent acinar atrophy, recent cases have shown significant functional acinar loss in the absence of apparent ductal keratinization or blockage. The deterioration of either MG obstruction or dropout exacerbates the condition of the other, suggesting an independent yet interconnected relationship that perpetuates the vicious cycle of MGD. Understanding the distinct pathological features of MG obstruction and dropout is crucial for delineating their etiology and identifying targeted therapeutic strategies. This review explores the nuanced interrelations of MG obstruction and dropout, elucidating potential pathological mechanisms to establish a foundation for early MGD diagnosis and intervention.

圆锥角膜（KC）是一种典型的扩张性眼病，以角膜扩张变薄并向前锥形突起为特征，严重时可致盲。KC三联征之一铁锈色Fleischer环，主要由上皮细胞基底膜周围的铁离子沉积组成。近年来，越来越多研究表明，铁稳态失衡可能与KC的发生和发展密切相关。KC患者泪液中铁相关蛋白的异常表达，提示铁稳态失衡可能是诱发KC的潜在致病机制。此外，角膜上皮细胞内铁稳态失衡导致细胞内铁离子异常积聚，进而引发活性氧和脂质过氧化物的大量生成，最终可能触发细胞铁死亡。从恢复铁稳态角度出发，螯合过量的铁离子和调控铁死亡过程关键靶点可能是未来KC潜在的治疗方法。目前关于铁稳态失衡导致KC发病的具体机制仍存在诸多谜团。随着相关研究的不断深入，有望通过改善角膜铁稳态失衡，为KC临床治疗带来新的思路和突破，也为KC患者提供更精准和个体化的治疗策略。

圆锥角膜（KC）是一种典型的扩张性眼病，以角膜扩张变薄并向前锥形突起为特征，严重时可致盲。KC三联征之一铁锈色Fleischer环，主要由上皮细胞基底膜周围的铁离子沉积组成。近年来，越来越多研究表明，铁稳态失衡可能与KC的发生和发展密切相关。KC患者泪液中铁相关蛋白的异常表达，提示铁稳态失衡可能是诱发KC的潜在致病机制。此外，角膜上皮细胞内铁稳态失衡导致细胞内铁离子异常积聚，进而引发活性氧和脂质过氧化物的大量生成，最终可能触发细胞铁死亡。从恢复铁稳态角度出发，螯合过量的铁离子和调控铁死亡过程关键靶点可能是未来KC潜在的治疗方法。目前关于铁稳态失衡导致KC发病的具体机制仍存在诸多谜团。随着相关研究的不断深入，有望通过改善角膜铁稳态失衡，为KC临床治疗带来新的思路和突破，也为KC患者提供更精准和个体化的治疗策略。