Evidence map›Paper›PMID 26136557›Full record

ReviewAmerican journal of physiology. Renal physiology2015

ABCG2: the molecular mechanisms of urate secretion and gout.

Owen M Woodward

Abstract readReview
In one paragraph

Review in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.2field-weighted citation impact, top 23% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. The Evolving Landscape of Gout in the Female: A Narrative Review.Gout, urate, and crystal deposition disease · 2023
    Article
  10. Article
  11. Review
  12. Combinatorial chemistry & high throughput screening · 2023
    Article
  13. Review
  14. Article
  15. Review
  16. Sex Differences in Urate Handling.International journal of molecular sciences · 2020
    Review
  17. Transcription factor-mediated regulation of the BCRP/Expert opinion on drug metabolism & toxicology · 2020
    Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Owen M WoodwardDepartment of Physiology, University of Maryland School of Medicine, Baltimore, Maryland OWoodward@som.umaryland.edu.
University of Maryland, Baltimore · US

Funding

Research BaseP30DK090868 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI WATNICK, TERRY J · 2010 to 2019
$11.1M
NIDDK NIH HHS P30 DK090868NIDDK NIH HHS P30DK090868
6 · The paper itself

Abstract

The human propensity for high levels of serum uric acid (SUA) is a trait that has defied explanation. Is it beneficial? Is it pathogenic? Its role in the human diseases like gout and kidney stones was discovered over a century ago [Richette P, Bardin T. Lancet 375: 318-328, 2010; Rivard C, Thomas J, Lanaspa MA, Johnson RJ. Rheumatology (Oxford) 52: 421-426, 2013], but today emerging new genetic and epidemiological techniques have revived an age-old debate over whether high uric acid levels (hyperuricemia) independently increase risk for diseases like hypertension and chronic kidney disease [Feig DI. J Clin Hypertens (Greenwich) 14: 346-352, 2012; Feig DI, Madero M, Jalal DI, Sanchez-Lozada LG, Johnson RJ. J Pediatr 162: 896-902, 2013; Feig DI, Soletsky B, Johnson RJ. JAMA 300: 924-932, 2008; Wang J, Qin T, Chen J, Li Y, Wang L, Huang H, Li J. PLoS One 9: e114259, 2014; Zhu P, Liu Y, Han L, Xu G, Ran JM. PLoS One 9: e100801, 2014]. Part of the mystery of the role uric acid plays in human health stems from our lack of understanding of how humans regulate uric acid homeostasis, an understanding that could shed light on the historic role of uric acid in human adaptation and its present role in human pathogenesis. This review will highlight the recent work to identify the first important human uric acid secretory transporter, ABCG2, and the identification of a common causal ABCG2 variant, Q141K, for hyperuricemia and gout.

Indexed as

ATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2GoutHumansHyperuricemiaModels, MolecularNeoplasm ProteinsProtein ConformationUric AcidABCG2 protein, humanATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2Neoplasm ProteinsUric AcidABCG2gouthyperuricemiakidneyQ141Kuric acid

Identifiers

PMID26136557
PMCPMC4572392
OpenAlexW1779125340

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.