Evidence map›Paper›PMID 23676498›Full record

ArticleThe Journal of clinical investigation2013

BMPR2 is required for postimplantation uterine function and pregnancy maintenance.

Takashi Nagashima, Qinglei Li, Caterina Clementi, John P Lydon, Francesco J DeMayo, Martin M Matzuk

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
8.4field-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

75 citing papers in PubMed, 121 citations in OpenAlex.

  1. Article
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  12. Endometrial TGFβ signaling fosters early pregnancy development by remodeling the fetomaternal interface.American journal of reproductive immunology (New York, N.Y. : 1989) · 2023
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Comparing the potential for maternal-fetal signalling in oviparous and viviparous lizards.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022
    Article
  18. Article
  19. The role of BMP4 signaling in trophoblast emergence from pluripotency.Cellular and molecular life sciences : CMLS · 2022
    Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Takashi NagashimaDepartment of Pathology and Immunology, Baylor College of Medicine, Houston, Texas 77030, USA.
Qinglei Li
Caterina Clementi
John P Lydon
Francesco J DeMayo
Martin M Matzuk
Baylor College of Medicine · USTexas A&M University · US

Funding

TRANSGENIC MOUSE MODELS TO STUDY OVARIAN FUNCTIONU54HD007495 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI MANCINI, MICHAEL A. · 1998 to 2013
$19.9M
Transforming growth factor β family signaling pathways in ovarian and uterine biologyR01HD032067 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI MARTIN M. MATZUK · 1994 to 2026
$9.9M
Molecular Analysis of Uterine ReceptivityR01HD042311 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI LYDON, JOHN P · 2009 to 2023
$4.8M
PROGESTERONE RECEPTOR IN BREAST DEVELOPMENT AND CANCERR01CA077530 · NCI · BAYLOR COLLEGE OF MEDICINE · PI LYDON, JOHN P · 2005 to 2008
$1.2M
PROGESTERONE RECEPTOR AND BREAST CANCERR29CA077530 · NCI · BAYLOR COLLEGE OF MEDICINE · PI LYDON, JOHN P · 1998 to 2004
$398k
NCI NIH HHS CA077530NCI NIH HHS R01 CA077530NCI NIH HHS R29 CA077530NICHD NIH HHS HD032067NICHD NIH HHS R01 HD032067NICHD NIH HHS R01 HD042311NICHD NIH HHS R01HD042311NICHD NIH HHS U54 HD007495NICHD NIH HHS U54HD007495
6 · The paper itself

Abstract

Abnormalities in cell-cell communication and growth factor signaling pathways can lead to defects in maternal-fetal interactions during pregnancy, including immunologic rejection of the fetal/placental unit. In this study, we discovered that bone morphogenetic protein receptor type 2 (BMPR2) is essential for postimplantation physiology and fertility. Despite normal implantation and early placental/fetal development, deletion of Bmpr2 in the uterine deciduae of mice triggered midgestation abnormalities in decidualization that resulted in abnormal vascular development, trophoblast defects, and a deficiency of uterine natural killer cells. Absence of BMPR2 signaling in the uterine decidua consequently suppressed IL-15, VEGF, angiopoietin, and corin signaling. Disruption of these pathways collectively lead to placental abruption, fetal demise, and female sterility, thereby placing BMPR2 at a central point in the regulation of several physiologic signaling pathways and events at the maternal-fetal interface. Since trophoblast invasion and uterine vascular modification are implicated in normal placentation and fetal growth in humans, our findings suggest that abnormalities in uterine BMPR2-mediated signaling pathways can have catastrophic consequences in women for the maintenance of pregnancy.

Indexed as

Embryo ImplantationPregnancy MaintenanceAngiopoietinsAnimalsBone Morphogenetic Protein Receptors, Type IICell DifferentiationCell ProliferationDeciduaEstradiolFemaleFetal Growth RetardationGene ExpressionGiant CellsInfertility, FemaleInterleukin-15Killer Cells, NaturalAngiopoietinsBmpr2 protein, mouseBone Morphogenetic Protein Receptors, Type IICorin protein, mouseEstradiolInterleukin-15ProgesteroneSerine EndopeptidasesVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouse

Identifiers

PMID23676498
PMCPMC3668851
OpenAlexW2052703349

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.