Evidence map›Paper›PMID 31875883›Full record

ArticleEndocrinology2020

The Autophagy Gene Atg16L1 is Necessary for Endometrial Decidualization.

Arin K Oestreich, Sangappa B Chadchan, Pooja Popli, Alexandra Medvedeva, Marina N Rowen, Claire S Stephens, Ran Xu, John P Lydon, Francesco J Demayo, Emily S Jungheim and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
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  9. Research Progress of Ribosomal Proteins in Reproductive Development.International journal of molecular sciences · 2024
    Review
  10. Article
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  15. Article
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  17. The Multifaceted Role of Autophagy in Endometrium Homeostasis and Disease.Reproductive sciences (Thousand Oaks, Calif.) · 2022
    Review
  18. Insight of Autophagy in Spontaneous Miscarriage.International journal of biological sciences · 2022
    Review
  19. Article
  20. Review
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

12 authors at 3 institutions in 1 country.

Arin K OestreichDepartment Obstetrics and Gynecology, Center for Reproductive Health Sciences, Washington University School of Medicine, St. Louis, Missouri.
Sangappa B ChadchanDepartment Obstetrics and Gynecology, Center for Reproductive Health Sciences, Washington University School of Medicine, St. Louis, Missouri.
Pooja PopliDepartment Obstetrics and Gynecology, Center for Reproductive Health Sciences, Washington University School of Medicine, St. Louis, Missouri.
Alexandra MedvedevaDepartment Obstetrics and Gynecology, Center for Reproductive Health Sciences, Washington University School of Medicine, St. Louis, Missouri.
Marina N RowenDepartment Obstetrics and Gynecology, Center for Reproductive Health Sciences, Washington University School of Medicine, St. Louis, Missouri.
Claire S StephensDepartment Obstetrics and Gynecology, Center for Reproductive Health Sciences, Washington University School of Medicine, St. Louis, Missouri.
Ran XuDepartment Obstetrics and Gynecology, Center for Reproductive Health Sciences, Washington University School of Medicine, St. Louis, Missouri.
John P LydonDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas.
Francesco J DemayoReproductive & Developmental Laboratory, National Institute of Environmental Health Sciences (NIEHS), Research Triangle Park, North Carolina.
Emily S JungheimDepartment Obstetrics and Gynecology, Center for Reproductive Health Sciences, Washington University School of Medicine, St. Louis, Missouri.
Kelle H MoleyDepartment Obstetrics and Gynecology, Center for Reproductive Health Sciences, Washington University School of Medicine, St. Louis, Missouri.
Ramakrishna KommaganiDepartment Obstetrics and Gynecology, Center for Reproductive Health Sciences, Washington University School of Medicine, St. Louis, Missouri.
Washington University in St. Louis · USBaylor College of Medicine · USNational Institute of Environmental Health Sciences · US

Funding

DIABETES &RELATED METABOLIC DISEASEST32DK007120 · NIDDK · WASHINGTON UNIVERSITY · PI MARCO COLONNA, Maria Sara Remedi · 1986 to 2026
$15.7M
Molecular Analysis of Uterine ReceptivityR01HD042311 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI LYDON, JOHN P · 2009 to 2023
$4.8M
MOLECULAR AND METABOLIC ASPECTS OF IMPLANTATIONR01HD065435 · NICHD · WASHINGTON UNIVERSITY · PI KOMMAGANI, RAMAKRISHNA, SANTI, CELIA M · 2010 to 2020
$4.5M
SLO3 KO MOUSE: A TOOL TO REVEAL VOLTAGE-DEPENDENT PROCESSES IN SPERM FERTILITYR01HD069631 · NICHD · WASHINGTON UNIVERSITY · PI SANTI, CELIA M · 2011 to 2022
$3.3M
Maternal nutrition and oocyte programmingR01HD083895 · NICHD · WASHINGTON UNIVERSITY · PI ENGLAND, SARAH K. · 2015 to 2019
$2.7M
GREB1 Action in Endometrial Function and DysfunctionR00HD080742 · NICHD · WASHINGTON UNIVERSITY · PI KOMMAGANI, RAMAKRISHNA · 2017 to 2019
$702k
NICHD NIH HHS R00 HD080742NICHD NIH HHS R01 HD042311NICHD NIH HHS R01 HD065435NICHD NIH HHS R01 HD069631NICHD NIH HHS R01 HD083895NIDDK NIH HHS T32 DK007120
6 · The paper itself

Abstract

Uterine receptivity is critical for establishing and maintaining pregnancy. For the endometrium to become receptive, stromal cells must differentiate into decidual cells capable of secreting factors necessary for embryo survival and placental development. Although there are multiple reports of autophagy induction correlated with endometrial stromal cell (ESC) decidualization, the role of autophagy in decidualization has remained elusive. To determine the role of autophagy in decidualization, we utilized 2 genetic models carrying mutations to the autophagy gene Atg16L1. Although the hypomorphic Atg16L1 mouse was fertile and displayed proper decidualization, conditional knockout in the reproductive tract of female mice reduced fertility by decreasing the implantation rate. In the absence of Atg16L1, ESCs failed to properly decidualize and fewer blastocysts were able to implant. Additionally, small interfering RNA knock down of Atg16L1 was detrimental to the decidualization response of human ESCs. We conclude that Atg16L1 is necessary for decidualization, implantation, and overall fertility in mice. Furthermore, considering its requirement for human endometrial decidualization, these data suggest Atg16L1 may be a potential mediator of implantation success in women.

Indexed as

MutationAnimalsAutophagyAutophagy-Related ProteinsCell DifferentiationCells, CulturedDeciduaEmbryo ImplantationEndometriumFemaleGene Expression Regulation, DevelopmentalHumansMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicAtg16l1 protein, mouseAutophagy-Related Proteinsfertilityimplantationpregnancy

Identifiers

PMID31875883
PMCPMC6986551
OpenAlexW2998152429

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.