Evidence map›Paper›PMID 27582104›Full record

ReviewAmerican journal of physiology. Renal physiology2017

Ironing out the cross talk between FGF23 and inflammation.

Valentin David, Connor Francis, Jodie L Babitt

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Renal physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

62 citing papers in PubMed, 109 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Effect of ferric citrate on serum phosphate and fibroblast growth factor 23 among patients with nondialysis-dependent chronic kidney disease: path analyses.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2019
    Trial
  4. Trial
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article

2 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Valentin DavidDivision of Nephrology and Hypertension, Department of Medicine, and Center for Translational Metabolism and Health, Institute for Public Health and Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois; and.
Connor FrancisDivision of Nephrology and Hypertension, Department of Medicine, and Center for Translational Metabolism and Health, Institute for Public Health and Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois; and.
Jodie L BabittNephrology Division, Program in Membrane Biology, and Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts Babitt.jodie@mgh.harvard.edu.
Northwestern University · USMassachusetts General Hospital · US

Funding

Regulation of Iron Homeostasis by BMP SignalingR01DK087727 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI BABITT, JODIE L · 2010 to 2024
$6.0M
Regulation of FGF23 in Chronic Kidney Disease (CKD) by iron and inflammationR01DK102815 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI DAVID, NICOLAE VALENTIN · 2015 to 2024
$4.9M
NIDDK NIH HHS R01 DK087727NIDDK NIH HHS R01 DK102815
6 · The paper itself

Abstract

The bone-secreted hormone fibroblast growth factor 23 (FGF23) has an essential role in phosphate homeostasis by regulating expression of the kidney proximal tubule sodium-phosphate cotransporters as well as parathyroid hormone levels. Induction of FGF23 early in chronic kidney disease (CKD) helps to maintain normal phosphorous levels. However, high FGF23 levels become pathological as kidney disease progresses and are associated with an increased risk of CKD progression, cardiovascular events, and death. The factors responsible for increasing FGF23 levels early in CKD are unknown, but recent work has proposed a role for inflammation and disordered iron homeostasis. Notably, FGF23 has recently been shown to elicit an inflammatory response and to display immunomodulatory properties. Here, we will review emerging evidence on the cross talk between inflammation, iron, FGF23, and bone and mineral metabolism and discuss the relevance for CKD patients.

Indexed as

AnimalsFibroblast Growth Factor-23Fibroblast Growth FactorsHomeostasisHumansInflammationKidneyParathyroid HormoneRenal Insufficiency, ChronicFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsParathyroid Hormonechronic kidney diseasefibroblast growth factor 23ironmineral metabolism

Identifiers

PMID27582104
PMCPMC5283889
OpenAlexW2517975681

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.