ArticleJournal of human genetics2023
GLUT9 as a potential drug target for chronic kidney disease: Drug target validation by a Mendelian randomization study.
Article in Journal of human genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed, 8 citations in OpenAlex.
- Urate-lowering therapy in cardiovascular pharmacotherapy: from Mendelian randomization data to cardio-renal-metabolic risk modulation.European heart journal. Cardiovascular pharmacotherapy · 2026Review
- Genetic and epigenetic contribution of ABCG2 to gout susceptibility: a case-control study.Molecular biology reports · 2025Article
- Reconstructing Molecular Networks by Causal Diffusion Do-Calculus Analysis with Deep Learning.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although chronic kidney disease (CKD) is recognized as a major public health concern, effective treatment strategies have yet to be developed. Identification and validation of drug targets are key issues in the development of therapeutic agents for CKD. Uric acid (UA), a major risk factor for gout, has also been suggested to be a risk factor for CKD, but the efficacy of existing urate-lowering therapies for CKD is controversial. We focused on five uric acid transporters (ABCG2, SLC17A1, SLC22A11, SLC22A12, SLC2A9) as potential drug targets and evaluated the causal association between serum UA levels and estimated glomerular filtration rate (eGFR) using single-SNP Mendelian Randomization. The results showed a causal association between genetically predicted changes in serum UA levels and eGFR when genetic variants were selected from the SLC2A9 locus. Estimation based on a loss-of-function mutation (rs16890979) showed that the changes in eGFR per unit increase in serum UA level was -0.0082 ml/min/1.73 m
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Registered trials
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