ArticleHereditas2024
Genetic insights into therapeutic targets for gout: evidence from a multi-omics mendelian randomization study.
Article in Hereditas, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- DNA Methylation Regulates CDK5R1 and NRBP1 to Exert Effects on Alcohol Dependence: Insights From Mendelian Randomization.Addiction biology · 2026Article
- Preliminary analysis of lifestyle and genetic factors for hyperuricemia and gout prevalence in the Yunnan Miao population of China.Frontiers in genetics · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundConsidering that the treatment of gout is poor, we performed a Mendelian randomization (MR) study to identify candidate biomarkers and therapeutic targets for gout.
methodsA drug-targeted MR study was performed for gout by integrating the gout genome-wide association studies (GWAS) summary data and cis expression quantitative trait loci of 2,633 druggable genes from multiple cohorts. Summary data-based Mendelian randomization (SMR) analyses based on transcript and protein levels were further implemented to validate the reliability of the identified potential therapeutic targets for gout. Phenome-wide MR (Phe-MR) analysis was conducted in 1403 diseases to investigate incidental side effects of potential therapeutic targets for gout.
resultsEight potential therapeutic targets (ALDH3B1, FCGR2B, IL2RB, NRBP1, RCE1, SLC7A7, SUMF1, THBS3) for gout were identified in the discovery cohort using MR analysis. Replication analysis and meta-analysis implemented in the replication cohort validated the robustness of the MR findings (P < 0.05). Evidence from the SMR analysis (P < 0.05) further strengthened the reliability of the 8 potential therapeutic targets for gout also revealed that high levels of ALDH3B1 reduced the gout risk possibly modified by the methylation site cg25402137. SMR analysis (P < 0.05) at the protein level added emphasis on the impact of the risk genes NRBP1 and SUMF1 on gout. Phe-MR analysis indicated significant causality between 7 gout causal genes and 45 diseases.
conclusionThis study identified several biomarkers associated with gout risk, providing new insights into the etiology of gout and promising targets for the development of therapeutic agents.
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