Identifying the important involvement of cuproptosis in the pathophysiology of age-related macular degeneration

Abstract Background Age-related macular degeneration (AMD) is a neurodegenerative disease associated with severe visual impairment in the elders. Despite recent studies and advances, the pathophysiology underlying the development of AMD is still not fully understood, and current therapies remain lim...

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Main Authors: Shizhen Lei, Yani Liu
Format: Article
Language:English
Published: BMC 2025-07-01
Series:European Journal of Medical Research
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Online Access:https://doi.org/10.1186/s40001-025-02818-7
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author Shizhen Lei
Yani Liu
author_facet Shizhen Lei
Yani Liu
author_sort Shizhen Lei
collection DOAJ
description Abstract Background Age-related macular degeneration (AMD) is a neurodegenerative disease associated with severe visual impairment in the elders. Despite recent studies and advances, the pathophysiology underlying the development of AMD is still not fully understood, and current therapies remain limited. Programmed cell death (PCD) has been implicated in neurodegenerative diseases. Therefore, the aim of this study is to investigate and identify key types of PCD and PCD-related genes involved in the pathogenesis of age-related macular degeneration (AMD). Methods This study employs transcriptomic analyses and animal experiments. For bulk tissue transcriptomic analysis, the enrichment scores of PCD forms in AMD samples were calculated using the single-sample gene set enrichment analysis (ssGSEA) algorithm. Single-cell transcriptomic analysis was conducted to examine the expression of PCD-related genes across different cell types. A mouse model was used to evaluate the therapeutic effects of a copper chelator on AMD. Results Enrichment analysis indicated that cuproptosis was the most enriched type of PCD process in both AMD-affected macular and retinal pigment epithelium (RPE) samples. In addition, cuproptosis was associated with the progression of AMD. Single-cell transcriptomic analysis revealed that cuproptosis was highly activated in varies retinal cells from AMD samples when compared to normal ones. Pathway enrichment analysis showed that cuproptosis was associated with angiogenesis, inflammation, and cellular senescence in AMD. Furthermore, the copper chelator demonstrated a protective effect on retinal function in the AMD mouse model. Conclusions Our findings identified an important role of cuproptosis in the pathophysiology of AMD and suggested the potential of cuproptosis as a therapeutic target for AMD.
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spelling doaj-art-e19a85a2f72f4a04a2f2e21f690f5e082025-08-20T03:04:23ZengBMCEuropean Journal of Medical Research2047-783X2025-07-0130111110.1186/s40001-025-02818-7Identifying the important involvement of cuproptosis in the pathophysiology of age-related macular degenerationShizhen Lei0Yani Liu1Department of Ophthalmology, Wuhan No. 1 HospitalDepartment of Otolaryngology and Head and Neck Surgery, Wuhan No.1 HospitalAbstract Background Age-related macular degeneration (AMD) is a neurodegenerative disease associated with severe visual impairment in the elders. Despite recent studies and advances, the pathophysiology underlying the development of AMD is still not fully understood, and current therapies remain limited. Programmed cell death (PCD) has been implicated in neurodegenerative diseases. Therefore, the aim of this study is to investigate and identify key types of PCD and PCD-related genes involved in the pathogenesis of age-related macular degeneration (AMD). Methods This study employs transcriptomic analyses and animal experiments. For bulk tissue transcriptomic analysis, the enrichment scores of PCD forms in AMD samples were calculated using the single-sample gene set enrichment analysis (ssGSEA) algorithm. Single-cell transcriptomic analysis was conducted to examine the expression of PCD-related genes across different cell types. A mouse model was used to evaluate the therapeutic effects of a copper chelator on AMD. Results Enrichment analysis indicated that cuproptosis was the most enriched type of PCD process in both AMD-affected macular and retinal pigment epithelium (RPE) samples. In addition, cuproptosis was associated with the progression of AMD. Single-cell transcriptomic analysis revealed that cuproptosis was highly activated in varies retinal cells from AMD samples when compared to normal ones. Pathway enrichment analysis showed that cuproptosis was associated with angiogenesis, inflammation, and cellular senescence in AMD. Furthermore, the copper chelator demonstrated a protective effect on retinal function in the AMD mouse model. Conclusions Our findings identified an important role of cuproptosis in the pathophysiology of AMD and suggested the potential of cuproptosis as a therapeutic target for AMD.https://doi.org/10.1186/s40001-025-02818-7Age-related macular degenerationProgrammed cell deathCuproptosisCopperSingle-cell RNA sequencing
spellingShingle Shizhen Lei
Yani Liu
Identifying the important involvement of cuproptosis in the pathophysiology of age-related macular degeneration
European Journal of Medical Research
Age-related macular degeneration
Programmed cell death
Cuproptosis
Copper
Single-cell RNA sequencing
title Identifying the important involvement of cuproptosis in the pathophysiology of age-related macular degeneration
title_full Identifying the important involvement of cuproptosis in the pathophysiology of age-related macular degeneration
title_fullStr Identifying the important involvement of cuproptosis in the pathophysiology of age-related macular degeneration
title_full_unstemmed Identifying the important involvement of cuproptosis in the pathophysiology of age-related macular degeneration
title_short Identifying the important involvement of cuproptosis in the pathophysiology of age-related macular degeneration
title_sort identifying the important involvement of cuproptosis in the pathophysiology of age related macular degeneration
topic Age-related macular degeneration
Programmed cell death
Cuproptosis
Copper
Single-cell RNA sequencing
url https://doi.org/10.1186/s40001-025-02818-7
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