Evidence map›Paper›PMID 25682045›Full record

ArticleJournal of cell communication and signaling2015

The role and regulation of IGFBP-1 phosphorylation in fetal growth restriction.

Madhulika B Gupta

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cell communication and signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Review
  3. Cord blood levels of insulin-like growth factor-1 and insulin-like growth factor binding protein-3 correlate with perinatal brain development in fetal congenital heart disease.Ultrasound in obstetrics & gynecology : the official journal of the International Society of Ultrasound in Obstetrics and Gynecology · 2025
    Observational
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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.

Madhulika B GuptaDepartments of Pediatrics and Biochemistry, Children's Health Research Institute, University of Western Ontario, VRL Room A5-136 (WC) 800 Commissioners Road E., London, ON, N6C 2V5, Canada, mbgupta@uwo.ca.
Western University · CA

Funding

Molecular Mechanisms Linking Placental Nutrient Sensing and Fetal ProgrammingR21HD071306 · NICHD · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI MYATT, LESLIE · 2012 to 2013
$378k
IGFBP-1 hyperphosphorylation in IUGR: Role of mTOR and CK2R03HD078313 · NICHD · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI GUPTA, MADHULIKA, JANSSON, THOMAS · 2014 to 2015
$147k
NICHD NIH HHS R03 HD078313NICHD NIH HHS R21 HD071306
6 · The paper itself

Abstract

Fetal growth restriction (FGR) increases the risk of perinatal complications and predisposes the infant to developing metabolic, cardiovascular, and neurological diseases in childhood and adulthood. The pathophysiology underlying FGR remains poorly understood and there is no specific treatment available. Biomarkers for early detection are also lacking. The insulin-like growth factor (IGF) system is an important regulator of fetal growth. IGF-I is the primary regulator of fetal growth, and fetal circulating levels of IGF-I are decreased in FGR. IGF-I activity is influenced by a family of IGF binding proteins (IGFBPs), which bind to IGF-I and decrease its bioavailability. During fetal development the predominant IGF-I binding protein in fetal circulation is IGFBP-1, which is primarily secreted by the fetal liver. IGFBP-1 binds IGF-I and thereby inhibits its bioactivity. Fetal circulating levels of IGF-I are decreased and concentrations of IGFBP-1 are increased in FGR. Phosphorylation of human IGFBP-1 at specific sites markedly increases its binding affinity for IGF-I, further limiting IGF-I bioactivity. Recent experimental evidence suggests that IGFBP-1 phosphorylation is markedly increased in the circulation of FGR fetuses suggesting an important role of IGFBP-1 phosphorylation in the regulation of fetal growth. Understanding of the significance of site-specific IGFBP-1 phosphorylation and how it is regulated to contribute to fetal growth will be an important step in designing strategies for preventing, managing, and/or treating FGR. Furthermore, IGFBP-1 hyperphosphorylation at unique sites may serve as a valuable biomarker for FGR.

Identifiers

PMID25682045
PMCPMC4458246
OpenAlexW2037969835

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.