Genetic prioritisation of candidate drug targets for glaucoma through multi-trait and multi-omics integration

Abstract Background Glaucoma causes permanent blindness. Current treatments have limited effectiveness, necessitating novel therapeutic strategies. We aimed to identify potential drug targets for glaucoma by integrating multi-trait and multi-omic analyses. Methods We sourced druggable gene expressio...

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Main Authors: Jianqi Chen, Yangjiani Li, Yingting Zhu, Zhidong Li, Shitong Huang, Wenzhi Huang, Yuyao Ling, Jingying Liang, Yunxia Leng, Yehong Zhuo
Format: Article
Language:English
Published: BMC 2025-07-01
Series:Eye and Vision
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Online Access:https://doi.org/10.1186/s40662-025-00442-4
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author Jianqi Chen
Yangjiani Li
Yingting Zhu
Zhidong Li
Shitong Huang
Wenzhi Huang
Yuyao Ling
Jingying Liang
Yunxia Leng
Yehong Zhuo
author_facet Jianqi Chen
Yangjiani Li
Yingting Zhu
Zhidong Li
Shitong Huang
Wenzhi Huang
Yuyao Ling
Jingying Liang
Yunxia Leng
Yehong Zhuo
author_sort Jianqi Chen
collection DOAJ
description Abstract Background Glaucoma causes permanent blindness. Current treatments have limited effectiveness, necessitating novel therapeutic strategies. We aimed to identify potential drug targets for glaucoma by integrating multi-trait and multi-omic analyses. Methods We sourced druggable gene expression and protein abundance summary-level data from quantitative trait loci studies, and genetic associations with glaucoma from a large-scale multi-trait analysis. We employed proteome and transcriptome Mendelian randomization (MR) and colocalisation to identify potential therapeutic targets, glaucoma endophenotype MR to explore the potential mechanisms of identified associations, and phenome-wide MR to investigate possible adverse effects of candidate targets. Results We identified CPXM1 and FLT4 as tier 1; INSR as tier 2; and CPZ and PXDN as tier 3 druggable genes. Genetically predicted higher levels of CPXM1 [odds ratio (OR): 0.86, 95% confidence interval (CI): 0.81–0.91, P FDR < 0.001], FLT4 (OR: 0.74, 95% CI: 0.64 − 0.87, P FDR = 0.033), INSR (OR: 0.58, 95% CI: 0.43 − 0.78, P FDR = 0.042), and CPZ (OR: 0.55, 95% CI: 0.40 − 0.74, P FDR = 0.033) were associated with decreased glaucoma risk while those of PXDN (OR: 1.33, 95% CI: 1.15 − 1.54, P FDR = 0.033) with increased risk. The associations for CPXM1 (OR: 0.53, 95% CI: 0.39 − 0.73, P < 0.001) and FLT4 (OR: 0.86, 95% CI: 0.78 − 0.95, P = 0.005) were confirmed transcriptome-wide and colocalisation was confirmed for CPXM1 [posterior probability H4 (PPH4) = 0.940], FLT4 (PPH4 = 0.701), and INSR (PPH4 = 0.706). The protective effects of CPXM1 and CPZ may be attributed to intraocular pressure-lowering activities. The risk associated with PXDN is due to its involvement in glaucomatous neuropathy. No significant adverse effects were identified. Conclusions This study provides novel insights into glaucoma pathophysiology and promotes pharmaceutical target innovation.
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spelling doaj-art-8bb0f1c801f44b5b9b97cb12a6ff4d302025-08-20T03:45:45ZengBMCEye and Vision2326-02542025-07-0112111410.1186/s40662-025-00442-4Genetic prioritisation of candidate drug targets for glaucoma through multi-trait and multi-omics integrationJianqi Chen0Yangjiani Li1Yingting Zhu2Zhidong Li3Shitong Huang4Wenzhi Huang5Yuyao Ling6Jingying Liang7Yunxia Leng8Yehong Zhuo9State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Sun Yat-Sen UniversityState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Sun Yat-Sen UniversityState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Sun Yat-Sen UniversityState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Sun Yat-Sen UniversityDepartment of Ophthalmology, Guangzhou First People’s Hospital, Guangzhou Medical UniversityDepartment of Ophthalmology, Guangzhou First People’s Hospital, Guangzhou Medical UniversityState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Sun Yat-Sen UniversityState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Sun Yat-Sen UniversityDepartment of Ophthalmology, Guangzhou First People’s Hospital, Guangzhou Medical UniversityState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Sun Yat-Sen UniversityAbstract Background Glaucoma causes permanent blindness. Current treatments have limited effectiveness, necessitating novel therapeutic strategies. We aimed to identify potential drug targets for glaucoma by integrating multi-trait and multi-omic analyses. Methods We sourced druggable gene expression and protein abundance summary-level data from quantitative trait loci studies, and genetic associations with glaucoma from a large-scale multi-trait analysis. We employed proteome and transcriptome Mendelian randomization (MR) and colocalisation to identify potential therapeutic targets, glaucoma endophenotype MR to explore the potential mechanisms of identified associations, and phenome-wide MR to investigate possible adverse effects of candidate targets. Results We identified CPXM1 and FLT4 as tier 1; INSR as tier 2; and CPZ and PXDN as tier 3 druggable genes. Genetically predicted higher levels of CPXM1 [odds ratio (OR): 0.86, 95% confidence interval (CI): 0.81–0.91, P FDR < 0.001], FLT4 (OR: 0.74, 95% CI: 0.64 − 0.87, P FDR = 0.033), INSR (OR: 0.58, 95% CI: 0.43 − 0.78, P FDR = 0.042), and CPZ (OR: 0.55, 95% CI: 0.40 − 0.74, P FDR = 0.033) were associated with decreased glaucoma risk while those of PXDN (OR: 1.33, 95% CI: 1.15 − 1.54, P FDR = 0.033) with increased risk. The associations for CPXM1 (OR: 0.53, 95% CI: 0.39 − 0.73, P < 0.001) and FLT4 (OR: 0.86, 95% CI: 0.78 − 0.95, P = 0.005) were confirmed transcriptome-wide and colocalisation was confirmed for CPXM1 [posterior probability H4 (PPH4) = 0.940], FLT4 (PPH4 = 0.701), and INSR (PPH4 = 0.706). The protective effects of CPXM1 and CPZ may be attributed to intraocular pressure-lowering activities. The risk associated with PXDN is due to its involvement in glaucomatous neuropathy. No significant adverse effects were identified. Conclusions This study provides novel insights into glaucoma pathophysiology and promotes pharmaceutical target innovation.https://doi.org/10.1186/s40662-025-00442-4Druggable targetsGlaucomaMulti-omicsMulti-traits
spellingShingle Jianqi Chen
Yangjiani Li
Yingting Zhu
Zhidong Li
Shitong Huang
Wenzhi Huang
Yuyao Ling
Jingying Liang
Yunxia Leng
Yehong Zhuo
Genetic prioritisation of candidate drug targets for glaucoma through multi-trait and multi-omics integration
Eye and Vision
Druggable targets
Glaucoma
Multi-omics
Multi-traits
title Genetic prioritisation of candidate drug targets for glaucoma through multi-trait and multi-omics integration
title_full Genetic prioritisation of candidate drug targets for glaucoma through multi-trait and multi-omics integration
title_fullStr Genetic prioritisation of candidate drug targets for glaucoma through multi-trait and multi-omics integration
title_full_unstemmed Genetic prioritisation of candidate drug targets for glaucoma through multi-trait and multi-omics integration
title_short Genetic prioritisation of candidate drug targets for glaucoma through multi-trait and multi-omics integration
title_sort genetic prioritisation of candidate drug targets for glaucoma through multi trait and multi omics integration
topic Druggable targets
Glaucoma
Multi-omics
Multi-traits
url https://doi.org/10.1186/s40662-025-00442-4
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