Evidence map›Paper›PMID 41088899›Full record

ArticleCombinatorial chemistry & high throughput screening2026

T1D-Related Cataract Risk Amplification: Mendelian Randomisation Confirms a Dual Hit of Immune-Inflammatory Burden and Metabolic Stress.

Xue Wang, Kunling Guo, Rui Li, Jiancen Tang, Wei Lou, Mengyu Wang, Wei Du, Hongping Cui, Qian Li

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Article in Combinatorial chemistry & high throughput screening, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Xue WangDepartment of Ophthalmology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200120, China.
Kunling GuoSchool of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Rui LiDepartment of Ophthalmology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200120, China.
Jiancen TangDepartment of Ophthalmology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200120, China.
Wei LouDepartment of Ophthalmology, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200233, China.
Mengyu WangDepartment of Ophthalmology, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200233, China.
Wei DuDepartment of Ophthalmology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200120, China.
Hongping CuiDepartment of Ophthalmology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200120, China.
Qian LiDepartment of Ophthalmology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200120, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectiveObservational studies have linked diabetes with cataracts, but they cannot fully elucidate the underlying causes and mechanisms. This investigation aims to evaluate the causal relationship between genetically predicted diabetes and cataract risk utilizing Mendelian randomisation (MR) techniques.

methodsWe identified single nucleotide polymorphisms (SNPs) with a significant threshold of P < 5×10^-8 as instrumental variables from genome-wide association study datasets pertaining to Type 1 (finn-b-E4_DM1, n=189,113), Type 2 diabetes (finn-b-E4_DM2, n=215,654), and cataract (ukb-b-8329, controls=136,388, cataract=14,254). Various Mendelian randomisation methods were employed, including inverse-variance weighted (IVW), MR-Egger, weighted median, simple mode (SM), and weighted mode analyses. Additionally, sensitivity analyses were conducted to assess the robustness of the findings, encompassing tests for heterogeneity, pleiotropy, and leave-one-out assessments. A multivariable (MVMR) approach was used to account for potential confounders, such as obesity (IEUA-92, controls = 47468, obesity = 2896), smoking (ukba- 16, n = 337030), and alcohol consumption (IEUA-1283, n = 112,117).

resultsThe analysis included 12 SNPs, which were derived from loci specifically associated with Type 1 diabetes and known to govern immune-inflammatory and metabolic pathways. The genetically-predicted Type 1 diabetes was found to elevate cataract risk significantly (OR=1.003, 95% CI: 1.001-1.005, P=0.001). The results of the sensitivity analyses corroborated the robustness of these findings, showing no significant heterogeneity (Cochran Q, P value = 0.73) or pleiotropy (MR-Egger intercept, P value = 0.38). Furthermore, multivariable MR demonstrated that the impact of diabetes on cataract risk remained significant after adjustment for multiple lifestyle factors. DISCUSSION: We provide novel MR evidence that Type 1 diabetes causally increases the risk of cataract through the synergistic activity of immune dysregulation, chronic inflammation, and metabolic disturbance, with immune-metabolic crosstalk as the primary driver.

conclusionsT1D causally increases the risk of cataract through the disruption of immuneinflammatory and metabolic pathways. Targeting immune-metabolic interactions may offer novel therapeutic strategies for preventing diabetic cataracts.

Indexed as

CataractDiabetes Mellitus, Type 1InflammationMendelian Randomization AnalysisStress, PhysiologicalGenome-Wide Association StudyHumansPolymorphism, Single NucleotideRisk Factorscataractcausal inferenceDiabetesimmune-inflammatory burdenlifestyle factorsmendelian randomisation

Identifiers

PMID41088899

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.