ArticleScientific reports2014
ABCG2 dysfunction causes hyperuricemia due to both renal urate underexcretion and renal urate overload.
Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 7 of them syntheses that pooled it.
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Who cites it
92 citing papers in PubMed, 7 syntheses or guidelines pooled it, 159 citations in OpenAlex.
- Discovery and prioritization of genetic determinants of kidney function in 297,355 individuals from Taiwan and Japan.Nature communications · 2024Pooled it
- Polygenic analysis of the effect of common and low-frequency genetic variants on serum uric acid levels in Korean individuals.Scientific reports · 2020Pooled it
- Subtype-specific gout susceptibility loci and enrichment of selection pressure onAnnals of the rheumatic diseases · 2020Pooled it
- A common variant of LDL receptor related protein 2 (LRP2) gene is associated with gout susceptibility: a meta-analysis in a Japanese population.Human cell · 2020Pooled it
- Genome-wide meta-analysis identifies multiple novel loci associated with serum uric acid levels in Japanese individuals.Communications biology · 2019Pooled it
- GWAS of clinically defined gout and subtypes identifies multiple susceptibility loci that include urate transporter genes.Annals of the rheumatic diseases · 2017Pooled it
- A meta-analysis of the associations between the Q141K and Q126X ABCG2 gene variants and gout risk.International journal of clinical and experimental pathology · 2015Pooled it
- Unraveling the genetic causes in large pedigrees with gout by whole‑exome sequencing.International journal of molecular medicine · 2020Trial
- Variants of ALPK1 with ABCG2, SLC2A9, and SLC22A12 increased the positive predictive value for gout.Journal of human genetics · 2018Trial
- Association between ABCG2 transporter functionality and CKD progression: a retrospective cohort study in patients with CKD stage G3.Clinical and experimental nephrology · 2026Article
- Redefining Uric Acid and Cardiovascular Risk: Vascular Gout and Crystal-Driven Vascular Inflammation in Asymptomatic Hyperuricemia.JACC. Asia · 2026Review
- Age- and sex-stratified serum reference intervals for eight trace elements in a large Japanese screening cohort.Journal of exposure science & environmental epidemiology · 2026Article
- ABCG2 transporter: Structural and functional associations with gout (Review).International journal of molecular medicine · 2026Review
- ABCG2 Genetic Variability in Drug Exposure and Toxicity: Implications for Clinical Practice.Toxics · 2026Review
- Synergistic effects of ABCG2 Q141K variant in combination with alcohol consumption and male sex on gout risk in a rare-event Taiwanese cohort.Scientific reports · 2026Article
- Regulatory mechanisms of programmed cell death in hyperuricaemia and their disease relevance.Frontiers in cell and developmental biology · 2026Review
- Article
- Dandelion Leaf Aqueous Extract Relieves Hyperuricemia and Its Complications via Modulating Uric Acid Metabolism, Renal Inflammation, and Gut Microbes.Foods (Basel, Switzerland) · 2025Article
- Hyperuricemia as an Early Indicator of Cardiovascular Risk in the General Population.Journal of clinical medicine · 2025Article
- Association of the ABCG2 Q141K variant with gout in Kinh Vietnamese: a cross-sectional study.Clinical rheumatology · 2025Article
32 more citing papers are in PubMed but not listed here.
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Authors and funding
27 authors at 9 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gout is a common disease which results from hyperuricemia. We have reported that the dysfunction of urate exporter ABCG2 is the major cause of renal overload (ROL) hyperuricemia, but its involvement in renal underexcretion (RUE) hyperuricemia, the most prevalent subtype, is not clearly explained so far. In this study, the association analysis with 644 hyperuricemia patients and 1,623 controls in male Japanese revealed that ABCG2 dysfunction significantly increased the risk of RUE hyperuricemia as well as overall and ROL hyperuricemia, according to the severity of impairment. ABCG2 dysfunction caused renal urate underexcretion and induced hyperuricemia even if the renal urate overload was not remarkable. These results show that ABCG2 plays physiologically important roles in both renal and extra-renal urate excretion mechanisms. Our findings indicate the importance of ABCG2 as a promising therapeutic and screening target of hyperuricemia and gout.
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