• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

视网膜疾病中铁代谢的研究进展

Research progress of iron metabolism in retinal diseases.

作者信息

Li Cunzi, Xiao Chunyu, Tao Hui, Tang Xianling

机构信息

Department of Ophthalmology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.

Department of Ophthalmology, Shenzhen Third People's Hospital, Shenzhen, China.

出版信息

Adv Ophthalmol Pract Res. 2023 Feb 28;3(2):93-100. doi: 10.1016/j.aopr.2023.02.001. eCollection 2023 May-Jun.

DOI:10.1016/j.aopr.2023.02.001
PMID:37846377
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10577842/
Abstract

BACKGROUND

Retinal diseases can lead to severe visual impairment and even blindness, but current treatments are limited. For precise targeted therapy, the pathophysiological mechanisms of the diseases still need to be further explored. Iron serves an essential role in many biological activities and helps maintain the function and morphology of the retina. The vision problems caused by retinal diseases are affecting more and more people, the study of iron metabolism in retinal diseases possesses great potential for clinical application.

MAIN TEXT

Iron maintains a dynamic balance in the retina but in excess is toxic to the retina. Iron overload can lead to various pathological changes in the retina through oxidative stress, inflammation, cell death, angiogenesis and other pathways. It is therefore involved in the progression of retinal diseases such as age-related macular degeneration, glaucoma, diabetic retinopathy, retinitis pigmentosa, and hereditary iron overload. In recent years, iron chelators have been shown to be effective in the treatment of retinal diseases, but the exact mechanism is not yet fully understood. This question prompted further investigation into the specific mechanisms by which iron metabolism is involved in retinal disease.

CONCLUSIONS

This review summarizes iron metabolism processes in the retina and mechanistic studies of iron metabolism in the progression of retinal disease. It also highlights the therapeutic potential of iron chelators in retinal diseases.

摘要

背景

视网膜疾病可导致严重的视力损害甚至失明,但目前的治疗方法有限。为了实现精准靶向治疗,仍需进一步探索这些疾病的病理生理机制。铁在许多生物活动中发挥着重要作用,并有助于维持视网膜的功能和形态。视网膜疾病引起的视力问题影响着越来越多的人,对视网膜疾病中铁代谢的研究具有巨大的临床应用潜力。

正文

铁在视网膜中维持动态平衡,但过量的铁对视网膜有毒性。铁过载可通过氧化应激、炎症、细胞死亡、血管生成等途径导致视网膜发生各种病理变化。因此,它参与了年龄相关性黄斑变性、青光眼、糖尿病视网膜病变、视网膜色素变性和遗传性铁过载等视网膜疾病的进展。近年来,铁螯合剂已被证明对视网膜疾病的治疗有效,但其确切机制尚未完全明确。这个问题促使人们进一步研究铁代谢参与视网膜疾病的具体机制。

结论

本综述总结了视网膜中的铁代谢过程以及铁代谢在视网膜疾病进展中的机制研究。它还强调了铁螯合剂在视网膜疾病中的治疗潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30c3/10577842/c8d33f94cac8/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30c3/10577842/c8d33f94cac8/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30c3/10577842/c8d33f94cac8/gr1.jpg

相似文献

1
Research progress of iron metabolism in retinal diseases.视网膜疾病中铁代谢的研究进展
Adv Ophthalmol Pract Res. 2023 Feb 28;3(2):93-100. doi: 10.1016/j.aopr.2023.02.001. eCollection 2023 May-Jun.
2
Potential Treatment of Retinal Diseases with Iron Chelators.铁螯合剂对视网膜疾病的潜在治疗作用
Pharmaceuticals (Basel). 2018 Oct 22;11(4):112. doi: 10.3390/ph11040112.
3
Revisiting Retinal Degeneration Hallmarks: Insights from Molecular Markers and Therapy Perspectives.重新审视视网膜变性的特征:分子标志物的启示和治疗观点。
Int J Mol Sci. 2023 Aug 23;24(17):13079. doi: 10.3390/ijms241713079.
4
Inflammation and retinal degenerative diseases.炎症与视网膜退行性疾病。
Neural Regen Res. 2023 Mar;18(3):513-518. doi: 10.4103/1673-5374.350192.
5
Cellular stress signaling and the unfolded protein response in retinal degeneration: mechanisms and therapeutic implications.细胞应激信号和未折叠蛋白反应在视网膜变性中的作用机制及治疗意义。
Mol Neurodegener. 2022 Mar 28;17(1):25. doi: 10.1186/s13024-022-00528-w.
6
[Visual impairment and blindness caused by posterior segment diseases in Hungary in people aged 50 years and older].[匈牙利50岁及以上人群后段疾病所致视力损害和失明情况]
Orv Hetil. 2022 Apr 17;163(16):624-630. doi: 10.1556/650.2022.32440.
7
Ferroptosis: mechanisms and advances in ocular diseases.铁死亡:眼疾的机制与新进展。
Mol Cell Biochem. 2023 Sep;478(9):2081-2095. doi: 10.1007/s11010-022-04644-5. Epub 2023 Jan 8.
8
Iron, zinc, and copper in retinal physiology and disease.视网膜生理学和疾病中的铁、锌、铜。
Surv Ophthalmol. 2013 Nov-Dec;58(6):585-609. doi: 10.1016/j.survophthal.2012.12.002.
9
Role of Oxidative Stress in Retinal Disease and the Early Intervention Strategies: A Review.氧化应激在视网膜疾病中的作用及早期干预策略:综述。
Oxid Med Cell Longev. 2022 Oct 14;2022:7836828. doi: 10.1155/2022/7836828. eCollection 2022.
10
Prospects of Stem Cells for Retinal Diseases.干细胞治疗视网膜疾病的前景。
Asia Pac J Ophthalmol (Phila). 2013 Jan-Feb;2(1):57-63. doi: 10.1097/APO.0b013e31827e3e5d.

引用本文的文献

1
Levels of Zinc, Iron, and Copper in the Aqueous Humor of Patients with Primary Glaucoma.原发性青光眼患者房水中锌、铁和铜的含量
Biomolecules. 2025 Jul 4;15(7):962. doi: 10.3390/biom15070962.
2
Retinal Complications in a Patient With Pediatric Thalassemia: A Case Report.一名小儿地中海贫血患者的视网膜并发症:病例报告
Cureus. 2025 Jun 23;17(6):e86610. doi: 10.7759/cureus.86610. eCollection 2025 Jun.
3
Dysregulation of Mitochondrial Iron Regulators as a Basis of Iron-Mediated Retinal Degeneration in Rats.线粒体铁调节因子失调作为大鼠铁介导视网膜变性的基础

本文引用的文献

1
Inhibition of ferroptosis promotes retina ganglion cell survival in experimental optic neuropathies.抑制铁死亡可促进实验性视神经病变中的视网膜神经节细胞存活。
Redox Biol. 2022 Dec;58:102541. doi: 10.1016/j.redox.2022.102541. Epub 2022 Nov 15.
2
Neuroprotective Effects of Transferrin in Experimental Glaucoma Models.转铁蛋白在实验性青光眼模型中的神经保护作用。
Int J Mol Sci. 2022 Oct 22;23(21):12753. doi: 10.3390/ijms232112753.
3
Research progress of ferroptosis in glaucoma and optic nerve damage.青光眼和视神经损伤中细胞铁死亡的研究进展
Neurotox Res. 2025 Jun 13;43(3):29. doi: 10.1007/s12640-025-00752-4.
4
Damage and repair in retinal degenerative diseases: Molecular basis through clinical translation.视网膜退行性疾病中的损伤与修复:从分子基础到临床转化
Neural Regen Res. 2026 Apr 1;21(4):1383-1395. doi: 10.4103/NRR.NRR-D-24-01016. Epub 2025 Feb 24.
5
Serum Iron Status and Retinal Degenerative Diseases: A Mendelian Randomization Study on AMD, RP, and DR.血清铁状态与视网膜退行性疾病:AMD、RP 和 DR 的孟德尔随机化研究。
Nutrients. 2024 Oct 31;16(21):3747. doi: 10.3390/nu16213747.
6
Recent Advances in Nanomedicine for Ocular Fundus Neovascularization Disease Management.纳米医学在眼部眼底新生血管疾病管理中的最新进展。
Adv Healthc Mater. 2024 Jul;13(17):e2304626. doi: 10.1002/adhm.202304626. Epub 2024 Mar 10.
Mol Cell Biochem. 2023 Apr;478(4):721-727. doi: 10.1007/s11010-022-04545-7. Epub 2022 Sep 2.
4
Pathologically high intraocular pressure disturbs normal iron homeostasis and leads to retinal ganglion cell ferroptosis in glaucoma.病理性高眼压扰乱了正常的铁稳态,导致青光眼患者的视网膜神经节细胞发生铁死亡。
Cell Death Differ. 2023 Jan;30(1):69-81. doi: 10.1038/s41418-022-01046-4. Epub 2022 Aug 6.
5
TRIM46 contributes to high glucose-induced ferroptosis and cell growth inhibition in human retinal capillary endothelial cells by facilitating GPX4 ubiquitination.TRIM46 通过促进 GPX4 泛素化促进高糖诱导的人视网膜毛细血管内皮细胞铁死亡和细胞生长抑制。
Exp Cell Res. 2021 Oct 15;407(2):112800. doi: 10.1016/j.yexcr.2021.112800. Epub 2021 Sep 4.
6
Effects of Iron and Zinc on Mitochondria: Potential Mechanisms of Glaucomatous Injury.铁和锌对线粒体的影响:青光眼性损伤的潜在机制
Front Cell Dev Biol. 2021 Aug 10;9:720288. doi: 10.3389/fcell.2021.720288. eCollection 2021.
7
Cell Ferroptosis: New Mechanism and New Hope for Retinitis Pigmentosa.细胞铁死亡:视网膜色素变性的新机制和新希望。
Cells. 2021 Aug 21;10(8):2153. doi: 10.3390/cells10082153.
8
ASYMPTOMATIC OCULAR MANIFESTATIONS OF ACERULOPLASMINEMIA IN TWO ADULT WHITE SIBLINGS: A MULTIMODAL IMAGING APPROACH.两例成年白化病兄弟的无症状眼型铜蓝蛋白血症:一种多模态成像方法。
Retin Cases Brief Rep. 2023 May 1;17(3):273-278. doi: 10.1097/ICB.0000000000001166. Epub 2021 May 17.
9
Glaucoma.青光眼。
Med Clin North Am. 2021 May;105(3):493-510. doi: 10.1016/j.mcna.2021.01.004. Epub 2021 Apr 2.
10
Potential of Application of Iron Chelating Agents in Ophthalmic Diseases.铁螯合剂在眼科疾病中的应用潜力。
Semin Ophthalmol. 2021 May 19;36(4):157-161. doi: 10.1080/08820538.2021.1887900. Epub 2021 Feb 23.