Evidence map›Paper›PMID 36650872›Full record

ArticleOpen veterinary journal

Vitamin D inhibited endometriosis development in mice model through interleukin-17 modulation.

Alfi Ruham Burjiah, Ashon Sa'adi, Widjiati Widjiati

Open access · goldAbstract read
In one paragraph

Article in Open veterinary journal. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Open veterinary journal · 2025
    Article
  3. Vitamin D and Endometriosis: Is There a Mechanistic Link?Cell biochemistry and function · 2025
    Review
  4. Article
  5. Review
  6. Vitamin DIn vitro cellular & developmental biology. Animal · 2024
    Article
  7. Review
  8. 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

3 authors at 1 institution in 1 country.

Alfi Ruham BurjiahPostgraduate Reproductive Health Science Study Program, Faculty of Medicine, Universitas Airlangga, Surabaya, Indonesia.
Ashon Sa'adiDepartment of Obstetrics and Gynecology, Faculty of Medicine, Universitas Airlangga, Surabaya, Indonesia.
Widjiati WidjiatiDepartment of Veterinary Science, Faculty of Veterinary Medicine, Universitas Airlangga, Surabaya, Indonesia.
Airlangga University · ID

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Endometriosis is a common, benign, estrogen-dependent, and chronic gynecological disease. Immune system disturbance and inflammatory abnormalities were involved in the pathogenesis of endometriosis. Therefore, it is logical to use vitamin D, which has an immunomodulatory capacity, as supportive therapy for endometriosis. Aim: This research aimed to study the effect of different doses of vitamin D on Interleukin-17 (IL-17) expression in endometriosis mice models. Methods: Endometriosis was induced in 24 mice divided into 4 groups of 6. Group C received no treatment, while groups T1, T2, and T3 received graded doses of oral vitamin D, sequentially 8, 16, and 24 IU, for 3 weeks. IL-17 expression and the extent of endometriotic peritoneal lesions were then measured and analyzed. Statistical tests were performed to see the difference in the mean area of endometriosis lesions and IL-17 expression between the control and treatment groups, as well as the correlation between the extent of endometriosis lesions and IL-17. Results: Endometriosis lesions decreased after 16 and 24 IU of vitamin D administration ( Conclusion: By modulating the expression of IL-17 in endometriotic lesions, vitamin D inhibited the development of endometriotic lesions in the endometriosis mice model. The recommended vitamin D dose in this study was 24 IU.

Indexed as

EndometriosisAnimalsDisease Models, AnimalFemaleInterleukin-17MiceVitamin DInterleukin-17Vitamin DEndometriosis lesionInterleukin-17ReproductiveVitamin D

Identifiers

PMID36650872
PMCPMC9805767
OpenAlexW4313229383

What OpenQuestion holds

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LicenceCC BY-NC
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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.