Evidence map›Paper›PMID 28883502›Full record

ArticleScientific reports2017

Activation of Endoplasmic Reticulum Stress in Granulosa Cells from Patients with Polycystic Ovary Syndrome Contributes to Ovarian Fibrosis.

Nozomi Takahashi, Miyuki Harada, Yasushi Hirota, Emi Nose, Jerilee Mk Azhary, Hiroshi Koike, Chisato Kunitomi, Osamu Yoshino, Gentaro Izumi, Tetsuya Hirata and 6 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 2 pooled it
7.9field-weighted citation impact, top 3% 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

63 citing papers in PubMed, 2 syntheses or guidelines pooled it, 116 citations in OpenAlex.

  1. Pooled it
  2. Adipose Tissue Dysfunction in Polycystic Ovary Syndrome.The Journal of clinical endocrinology and metabolism · 2023
    Pooled it
  3. Trial
  4. Trial
  5. Review
  6. Multimodal ultrasound assessment of ovarian reserve.Abdominal radiology (New York) · 2026
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Molecular mechanisms of ovarian fibrosis.Molecular human reproduction · 2026
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

3 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

16 authors at 3 institutions in 2 countries.

Nozomi TakahashiDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo, Tokyo, 113-8655, Japan.
Miyuki HaradaDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo, Tokyo, 113-8655, Japan. haradam-tky@umin.ac.jp.
Yasushi HirotaDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo, Tokyo, 113-8655, Japan.ORCID 0000-0003-0241-9780
Emi NoseDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo, Tokyo, 113-8655, Japan.
Jerilee Mk AzharyDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo, Tokyo, 113-8655, Japan.
Hiroshi KoikeDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo, Tokyo, 113-8655, Japan.
Chisato KunitomiDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo, Tokyo, 113-8655, Japan.
Osamu YoshinoDepartment of Obstetrics and Gynecology, Faculty of Medicine, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.
Gentaro IzumiDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo, Tokyo, 113-8655, Japan.
Tetsuya HirataDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo, Tokyo, 113-8655, Japan.
Kaori KogaDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo, Tokyo, 113-8655, Japan.
Osamu Wada-HiraikeDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo, Tokyo, 113-8655, Japan.
R Jeffrey ChangDepartment of Reproductive Medicine, University of California San Diego, 9500 Gilman Drive, La Jolla, CA, 92093-0633, USA.
Shunichi ShimasakiDepartment of Reproductive Medicine, University of California San Diego, 9500 Gilman Drive, La Jolla, CA, 92093-0633, USA.
Tomoyuki FujiiDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo, Tokyo, 113-8655, Japan.
Yutaka OsugaDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo, Tokyo, 113-8655, Japan.
The University of Tokyo · JPUniversity of California San Diego · USUniversity of Toyama · JP

Funding

The Interaction of Neuroendocrine Repro. Function and Metabolic SignalingU54HD012303 · NICHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MELLON, PAMELA L · 1999 to 2013
$18.0M
The Role of FSH in Female InfertilityP50HD012303 · NICHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LAWSON, MARK ANDREW · 1985 to 2020
$7.5M
NICHD NIH HHS P50 HD012303NICHD NIH HHS U54 HD012303
6 · The paper itself

Abstract

Recent studies report the involvement of intra-ovarian factors, such as inflammation and oxidative stress, in the pathophysiology of polycystic ovary syndrome (PCOS), the most common endocrine disorder of reproductive age women. Endoplasmic reticulum (ER) stress is a local factor that affects various cellular events during a broad spectrum of physiological and pathological conditions. It may also be an important determinant of pro-fibrotic remodeling during tissue fibrosis. In the present study, we showed that ER stress was activated in granulosa cells of PCOS patients as well as in a well-established PCOS mouse model. Pharmacological inducers of ER stress, tunicamycin and thapsigargin, were found to increase the expression of pro-fibrotic growth factors, including transforming growth factor (TGF)-β1, in human granulosa cells, and their expression also increased in granulosa cells of PCOS patients. By contrast, treatment of PCOS mice with an ER stress inhibitor, tauroursodeoxycholic acid or BGP-15, decreased interstitial fibrosis and collagen deposition in ovaries, accompanied by a reduction in TGF-β1 expression in granulosa cells. These findings suggest that ER stress in granulosa cells of women with PCOS contributes to the induction of pro-fibrotic growth factors during ovarian fibrosis, and that ER stress may serve as a therapeutic target in PCOS.

Indexed as

Endoplasmic Reticulum StressAnimalsCells, CulturedCollagenDisease Models, AnimalFemaleFibrosisGranulosa CellsHumansMiceOvaryPolycystic Ovary SyndromeTransforming Growth Factor beta1CollagenTransforming Growth Factor beta1

Identifiers

PMID28883502
PMCPMC5589802
OpenAlexW2751619916

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Registered trials

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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.