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. 

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。

目的：探讨无糖尿病性视网膜病变(diabetic retinopathy，DR)的糖尿病人群中，糖尿病与近视对黄斑区节细胞-内丛状层(ganglion cell layer and inner plexiform layer，GCIPL)厚度纵向变化的影响。方法：纳入广州糖尿病眼病研究中1165名基线无视网膜病变的糖尿病和正常对照者，纵向随访2年。根据是否存在近视[等效球镜(spherical equivalent，SE)≤-3屈光度(diopter，D)]和糖尿病分为健康组(n=508)、糖尿病组(n=525)及糖尿病合并近视组(n=132)。扫频光学相干断层成像(swept source-optical coherence tomography，SS-OCT)技术测量并比较三组间GCIPL厚度的变化，以确定糖尿病和近视的影响，三组间差异使用协方差分析，采用线性混合模型分析评估GCIPL厚度与相关因素的关系。结果：对照组的SE为(1.07±1.06) D，糖尿病组为(1.02±1.00) D，糖尿病合并近视组为(-5.36±2.30) D，组间差异有统计学意义(P<0.001)。对照组基线GCIPL厚度为(71.1±0.3) μm，糖尿病组为(74.4±0.2)μm，糖尿病合并近视组为(71.7±0.5) μm。在2年随访过程中，对照组GCIPL厚度下降-0.10(95%CI：-2.03~0.05) μm/年，糖尿病组GCIPL厚度下降的速度为对照组的12倍[-1.21(95%CI：-24.04~0.05) μm/年，P<0.001]，糖尿病合并近视组GCIPL厚度下降的速度为对照组的22倍[-2.17(95%CI：-21.63~0.10)μm/年，P<0.001]。结论：近视是无DR的糖尿病患者中GCIPL加速变薄的危险因素，糖尿病和近视在GCIPL损伤中可能存在协同作用。

Objective: To investigate the association between myopia and ganglion cell layer and inner plexiform layer (GCIPL) in diabetic population without diabetic retinopathy (DR). Methods: In this Guangzhou Diabetic Eye study, a total of 1 165 patients aged 30–80 years were recruited followed up longitudinally for 2 years. According to the presence or absence of myopia [spherical equivalence (SE)≤-3 diopter (D)] and diabetics, the patients were divided into a healthy group (n=508), a diabetes mellitus group (n=525), and a diabetes mellitus + myopia group (n=132). GCIPL was measured via swept-source optical coherence tomography. Univariable and multivariable mixed models were used to show the association of GCIPL change and baseline parameters. Results: SE was (1.07±1.06) D in the healthy group, (1.02±1.00) D in the diabetes mellitus group and (-5.36±2.30) D in the diabetes mellitus + myopia group (P<0.001). The baseline GCIPL thickness were (71.1±0.3), (74.4±0.2), and (71.7±0.5) μm, respectively. The slope of GCIPL thickness was -0.10 (95% CI: -2.03 to 0.05) μm/year in the healthy group, which was 12 folds faster than those in the diabetes mellitus group [-1.21(95% CI: -24.04 to 0.05 μm/year, P<0.001] and 22 folds higher among those in diabetes mellitus + myopia group [-2.17 (95% CI: -21.63 to 0.10) μm/year, P=0.009]. Conclusion: Both myopia and diabetes status accelerate macular ganglion cell layer and inner plexiform layer thinning in diabetic patients without diabetic retinopathy.

目的：探讨无糖尿病性视网膜病变(diabetic retinopathy，DR)的糖尿病人群中，糖尿病与近视对黄斑区节细胞-内丛状层(ganglion cell layer and inner plexiform layer，GCIPL)厚度纵向变化的影响。方法：纳入广州糖尿病眼病研究中1 165名基线无视网膜病变的糖尿病和正常对照者，纵向随访2年。根据是否存在近视[等效球镜(spherical equivalent，SE)≤-3 屈光度(diopter，D)]和糖尿病分为健康组(n =508)、糖尿病组(n =525)及糖尿病合并近视组(n =132)。扫频光学相干断层成像(swept source-optical coherence tomography，SS-OCT)技术测量并比较三组间GCIPL厚度的变化，以确定糖尿病和近视的影响，三组间差异使用协方差分析，采用线性混合模型分析评估GCIPL厚度与相关因素的关系。结果：对照组的SE为(1.07±1.06) D，糖尿病组为(1.02±1.00) D，糖尿病合并近视组为(-5.36±2.30D)，组间差异有统计学意义(P<0.001)。对照组基线GCIPL厚度为(71.1±0.3) μm，糖尿病组为(74.4±0.2) μm，糖尿病合并近视组为(71.7±0.5) μm。在2年随访过程中，对照组GCIPL厚度下降-0.10(95%CI：0.05~-2.03) μm/年，糖尿病组GCIPL厚度下降的速度为对照组的12倍[-1.21(95%CI：0.05~?24.04) μm/年，P<0.001]，糖尿病合并近视组GCIPL厚度下降的速度为对照组的22倍[-2.17(95%CI：0.10~-21.63) μm/年，P<0.001]。结论：近视是无DR的糖尿病患者中GCIPL加速变薄的危险因素，糖尿病和近视GCIPL损伤中可能存在协同作用。

Objective: To investigate the association between myopia and ganglion cell layer and inner plexiform layer(GCIPL) in diabetic population without diabetic retinopathy (DR). Methods: In this Guangzhou Diabetic Eyestudy, a total of 1165 patients aged 30–80 years were recruited followed up longitudinally for 2 years. According tothe presence or absence of myopia [spherical equivalence (SE)≤-3 diopter (D)] and diabetics, the patients weredivided into a healthy group (n=508), a diabetes mellitus group (n=525), and a diabetes mellitus + myopia group(n=132). GCIPL was measured via swept-source optical coherence tomography. Univariable and multivariablemixed models were used to show the association of GCIPL change and baseline parameters. Results: SE was(1.07±1.06) D in the healthy group, (1.02±1.00) D in the diabetes mellitus group and (-5.36±2.30) D in thediabetes mellitus + myopia group (P<0.001). The baseline GCIPL thickness were (71.1±0.3), (74.4±0.2), and(71.7±0.5) μm, respectively. The slope of GCIPL thickness was ?0.10 (95% CI: 0.05 to -2.03) μm/year in the healthy group, which was 12 folds faster than those in the diabetes mellitus group [-1.21(95% CI: 0.05 to-24.04) μm/year, P<0.001] and 22 folds higher among those in diabetes mellitus + myopia group [-2.17 (95%CI: 0.10 to ?21.63) μm/year, P=0.009]. Conclusion: Both myopia and diabetes status accelerate macular ganglioncell layer and inner plexiform layer thinning in diabetic patients without diabetic retinopathy.