Evidence map›Paper›PMID 19282364›Full record

ReviewMolecular endocrinology (Baltimore, Md.)2009

Minireview: fetal-maternal hormonal signaling in pregnancy and labor.

Carole R Mendelson

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Molecular endocrinology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
11.1field-weighted citation impact, top 1% 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

125 citing papers in PubMed, 282 citations in OpenAlex.

  1. Trial
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  5. Association betweenFrontiers in cellular and infection microbiology · 2025
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  18. Maternal H-antigen secretor status is an early biomarker for potential preterm delivery.Journal of perinatology : official journal of the California Perinatal Association · 2021
    Article
  19. Article
  20. Article

65 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

1 author at 1 institution in 1 country.

Carole R MendelsonDepartments of Biochemistry and Obstetrics and Gynecology, North Texas March of Dimes Birth Defects Center, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390-9038, USA. carole.mendelson@utsouthwestern.edu
The University of Texas Southwestern Medical Center · US

Funding

TRANSCRIPTIONAL REGULATION OF CERVICAL COMPETENCE DURING PREGNANCYP01HD011149 · NICHD · UT SOUTHWESTERN MEDICAL CENTER · PI MENDELSON, CAROLE R · 1998 to 2015
$17.7M
MECHANISMS IN THE REGULATION OF SP-A GENE EXPRESSIONR37HL050022 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI MENDELSON, CAROLE R. · 1998 to 2007
$3.2M
NHLBI NIH HHS R37 HL050022NICHD NIH HHS 5 P01 HD011149NICHD NIH HHS P01 HD011149
6 · The paper itself

Abstract

Mechanisms underlying the initiation of parturition remain unclear. Throughout most of pregnancy, uterine quiescence is maintained by elevated progesterone acting through progesterone receptor (PR). Although in most mammals, parturition is associated with a marked decline in maternal progesterone, in humans, circulating progesterone and uterine PR remain elevated throughout pregnancy, suggesting a critical role for functional PR inactivation in the initiation of labor. Both term and preterm labor in humans and rodents are associated with an inflammatory response. In preterm labor, intraamniotic infection likely provides the stimulus for increased amniotic fluid interleukins and migration of inflammatory cells into the uterus and cervix. However, at term, the stimulus for this inflammatory response is unknown. Increasing evidence suggests that the developing fetus may produce physical and hormonal signals that stimulate macrophage migration to the uterus, with release of cytokines and activation of inflammatory transcription factors, such as nuclear factor kappaB (NF-kappaB) and activator protein 1 (AP-1), which also is activated by myometrial stretch. We postulate that the increased inflammatory response and NF-kappaB activation promote uterine contractility via 1) direct activation of contractile genes (e.g. COX-2, oxytocin receptor, and connexin 43) and 2) impairment of the capacity of PR to mediate uterine quiescence. PR function near term may be compromised by direct interaction with NF-kappaB, altered expression of PR coregulators, increased metabolism of progesterone within the cervix and myometrium, and increased expression of inhibitory PR isoforms. Alternatively, we propose that uterine quiescence during pregnancy is regulated, in part, by PR antagonism of the inflammatory response.

Indexed as

Endocrine SystemFemaleHormonesHumansInflammationLabor, ObstetricMaternal-Fetal ExchangeModels, BiologicalPregnancySignal TransductionHormones

Identifiers

PMID19282364
PMCPMC2703595
OpenAlexW2155495754

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.