ArticleAntioxidants (Basel, Switzerland)2024
Causal Effects of Oxidative Stress on Diabetes Mellitus and Microvascular Complications: Insights Integrating Genome-Wide Mendelian Randomization, DNA Methylation, and Proteome.
Article in Antioxidants (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed.
- Uncovering Potential Druggable Targets in Coronary Atherosclerosis: A Proteome-Wide Mendelian Randomization Study With Cross-Platform and Experimental Validation.Cardiovascular therapeutics · 2026Article
- Multi-omics and comprehensive multi-trait analysis identify shared genetic etiology of heart failure and related cancers.Human genomics · 2025Article
- Understanding Atopic Dermatitis: Pathophysiology and Management Strategies.Biomolecules · 2025Review
- Liquid Biopsy Combined with Multi-Omics Approaches in Diagnosis, Management, and Progression of Diabetic Retinopathy.Biomedicines · 2025Review
- Impact of Type 1 Diabetes on Testicular Microtubule Dynamics, Sperm Physiology, and Male Reproductive Health in Rat.International journal of molecular sciences · 2025Article
- The contribution of dietary total antioxidant capacity to type 2 diabetes risk and levels of glycemic biomarkers: a systematic review.Osong public health and research perspectives · 2025Article
- Causal Impacts of Psychiatric Disorders on Cognition and the Mediating Effect of Oxidative Stress: A Mendelian Randomization Study.Antioxidants (Basel, Switzerland) · 2025Article
- Integrating plasma proteomics and genome-wide association data to identify therapeutic targets for retinal neurodegenerative diseases in Europeans.International journal of ophthalmology · 2025Article
- Association of Albumin-To-Creatinine Ratio With Diabetic Retinopathy Among US Adults (NHANES 2009-2016).Endocrinology, diabetes & metabolism · 2025Article
- Advances in the Epigenetic Mechanisms of Diabetic Nephropathy Pathogenesis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Review
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7 authors.
Funding
Abstract
backgroundOxidative stress (OS) is involved in the development of diabetes, but the genetic mechanisms are not completely understood. We integrated multi-omics data in order to explore the genetic relations between OS-related genes, diabetes mellitus, and microvascular complications using Mendelian randomization and colocalization analysis.
methodsSummary-level data related to OS were acquired from respective studies of methylation, expression, and protein abundance quantitative trait loci. Genetic associations concerning diabetes, diabetic nephropathy (DN), and diabetic retinopathy (DR) were derived from the FinnGen study. Summary-data-based Mendelian randomization (SMR) analysis was conducted to evaluate the correlations between molecular features concerned with OS-related genes and diabetes mellitus, along with its microvascular complications. Additionally, we performed colocalization analysis to determine if the detected signal pairs shared a causal genetic variant.
resultsAt the genetic level, we identified ten potential causal associations of oxidative stress genes with diabetes, along with microvascular complications, through SMR and colocalization analysis. After integrating the DNA methylation quantitative trait loci (mQTL) and expression QTL (eQTL) data, our analyses revealed a correlation between the methylation site cg26343298 and reduced expression of TP53INP1, supporting the protective role of cg26343298 methylation on type 2 diabetes (T2D) and diabetic nephropathy. Similarly, an inverse association was observed between gene methylation and expression in CHEK1 (cg07110182), confirming the beneficial effect of modification of CHEK1 by cg07110182 in diabetic retinopathy. In addition, upregulation of SUOX expression by cg22580629 was linked to a reduced risk of diabetic retinopathy. At circulating protein levels, genetically predicted a higher level of ICAM1 (OR 1.05, 95%CI 1.03-1.08) was positively connected with the risk of diabetic retinopathy.
conclusionsThis SMR study elucidated that the TP53INP1 gene was putatively associated with T2D and DN risk, while the SUOX and CHEK1 genes were associated with DR risk through oxidative stress mechanisms. Additionally, our study showed a positive correlation between the ICAM-1 protein and DR. These findings may enhance our understanding of their pathogenesis and suggest new therapeutic targets for clinical practice.
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