Evidence map›Paper›PMID 22728930›Full record

ArticleThe Journal of clinical investigation2012

Fibroblast growth factor 23: friend or foe in uremia?

Orson W Moe

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Strategies to lower fibroblast growth factor 23 bioactivity.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2022
    Article
  3. Review
  4. Article
  5. Review
  6. Phosphate Toxicity in CKD: The Killer among Us.Clinical journal of the American Society of Nephrology : CJASN · 2016
    Review
  7. NFκB-sensitive Orai1 expression in the regulation of FGF23 release.Journal of molecular medicine (Berlin, Germany) · 2016
    Article
  8. Article
  9. Article
  10. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author.

Orson W Moe

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Uremia is a complex metabolic state marked by derangement of many signaling molecules and metabolic intermediates; of these, the massively increased levels of FGF23 are among the most striking. It has remained unclear whether FGF23 is directly implicated in the pathogenesis of chronic kidney disease (CKD) and its complications, a consequence of other dysregulated pathways, or perhaps an adaptive - and thus desirable - response. In this issue of the JCI, Shalhoub et al. describe the chronic effects of antibody-mediated FGF23 neutralization in a CKD mouse model, shedding new light on this complicated story and moving us one step closer to understanding the role of FGF23 in CKD.

Indexed as

AnimalsFibroblast Growth Factor-23Fibroblast Growth FactorsHyperparathyroidism, SecondaryMaleRenal Insufficiency, ChronicFgf23 protein, mouseFgf23 protein, ratFibroblast Growth Factor-23Fibroblast Growth Factors

Identifiers

PMID22728930
PMCPMC3386835
OpenAlexW1983038989

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.