ReviewAsian journal of pharmaceutical sciences2020
Pharmacologic inducers of the uric acid exporter ABCG2 as potential drugs for treatment of gouty arthritis.
Review in Asian journal of pharmaceutical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 58 citations in OpenAlex.
- ABCG2 transporter: Structural and functional associations with gout (Review).International journal of molecular medicine · 2026Review
- Biomaterial-Based Strategies for Gout Therapy: Recent Advances, Current Challenges, and Future Perspectives - A Review.International journal of nanomedicine · 2026Review
- First case report of hypouricemia associated with adjuvant imatinib therapy in a patient with small intestinal gastrointestinal stromal tumor.Frontiers in oncology · 2026Article
- Review
- Effect of Probiotic Product Containing Heyndrickxia coagulans TBC169 on Hyperuricemia in Rats.Probiotics and antimicrobial proteins · 2026Article
- Short-term dynamics of serum uric acid and its influencing factors in patients with obesity after laparoscopic sleeve gastrectomy.BMC surgery · 2025Article
- Genetic variants associated with gout identified through a genome-wide study in the UK biobank (N = 150 542).Human molecular genetics · 2025Article
- Microalgae-based hydrogel drug delivery system for treatment of gouty arthritis with alleviated colchicine side effects.Bioactive materials · 2025Article
- Effects of hydroxypropyl starch on intestinal health and transcriptome of geese.Scientific reports · 2025Article
- Inhibition of METTL3 Attenuates Renal Fibrosis by Upregulating ABCG2 m6A Modifications via IGF2BP2-Dependent Mechanisms in Hyperuricemic Nephropathy.Journal of cellular and molecular medicine · 2025Article
- Drug-Induced Hypouricemia.Drug safety · 2025Review
- Severity and Prognosis of Vascular Dementia in Patients with Acute Cerebral Infarction Combined with H-Type Hypertension and Its Correlation with Uric Acid Levels.Neuropsychiatric disease and treatment · 2025Article
- A systems immunology perspective on gout pathogenesis and its precision-targeted treatment strategies.Frontiers in immunology · 2025Review
- Wuling capsule alleviates hyperuricaemia and protects UA- injured HK-2 cells by regulating uric acid transporter proteins.Frontiers in pharmacology · 2025Article
- Exercise and hyperuricemia: an opinion article.Annals of medicine · 2024Article
- Exploring the molecular mechanisms and shared potential drugs between rheumatoid arthritis and arthrofibrosis based on large language model and synovial microenvironment analysis.Scientific reports · 2024Article
- Emerging Urate-Lowering Drugs and Pharmacologic Treatment Strategies for Gout: A Narrative Review.Drugs · 2023Review
- Article
- Assessment of phytotoxic, genotoxic and enzyme inhibition potential of.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2022Article
- Hyperuricemia and the small intestine: Transport mechanisms and co-morbidities.Biotechnology notes (Amsterdam, Netherlands) · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Uric acid is the end product of purine catabolism and its plasma levels are maintained below its maximum solubility in water (6-7 mg/dl). The plasma levels are tightly regulated as the balance between the rate of production and the rate of excretion, the latter occurring in urine (kidney), bile (liver) and feces (intestinal tract). Reabsorption in kidney is also an important component of this process. Both excretion and reabsorption are mediated by specific transporters. Disruption of the balance between production and excretion leads to hyperuricemia, which increases the risk of uric acid crystallization as monosodium urate with subsequent deposition of the crystals in joints causing gouty arthritis. Loss-of-function mutations in the transporters that mediate uric acid excretion are associated with gout. The ATP-Binding Cassette exporter ABCG2 is important in uric acid excretion at all three sites: kidney (urine), liver (bile), and intestine (feces). Mutations in this transporter cause gout and these mutations occur at significant prevalence in general population. However, mutations that are most prevalent result only in partial loss of transport function. Therefore, if the expression of these partially defective transporters could be induced, the increased number of the transporter molecules would compensate for the mutation-associated decrease in transport function and hence increase uric acid excretion. As such, pharmacologic agents with ability to induce the expression of ABCG2 represent potentially a novel class of drugs for treatment of gouty arthritis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.