Evidence map›Paper›PMID 38645639›Full record

ReviewReproductive medicine and biology

Molecular mechanism of autophagy and apoptosis in endometriosis: Current understanding and future research directions.

Hiroshi Kobayashi, Shogo Imanaka, Chiharu Yoshimoto, Sho Matsubara, Hiroshi Shigetomi

Open access · goldAbstract readReview
In one paragraph

Review in Reproductive medicine and biology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
16.6field-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

27 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Endometriosis and the Hallmarks of Cancer.Reproductive sciences (Thousand Oaks, Calif.) · 2026
    Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
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  19. MEIS1-mediated Apoptosis via TNFR1 in Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2025
    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

5 authors at 3 institutions in 1 country.

Hiroshi KobayashiDepartment of Gynecology and Reproductive Medicine Ms.Clinic MayOne Kashihara Japan.ORCID https://orcid.org/0000-0002-8124-6269
Shogo ImanakaDepartment of Gynecology and Reproductive Medicine Ms.Clinic MayOne Kashihara Japan.
Chiharu YoshimotoDepartment of Obstetrics and Gynecology Nara Medical University Kashihara Japan.
Sho MatsubaraDepartment of Obstetrics and Gynecology Nara Medical University Kashihara Japan.
Hiroshi ShigetomiDepartment of Obstetrics and Gynecology Nara Medical University Kashihara Japan.
Nara Medical University · JPHyogo Prefectural Nishinomiya Hospital · JPNara Prefecture General Medical Center

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Endometriosis is a common gynecological condition, with symptoms including pain and infertility. Regurgitated endometrial cells into the peritoneal cavity encounter hypoxia and nutrient starvation. Endometriotic cells have evolved various adaptive mechanisms to survive in this inevitable condition. These adaptations include escape from apoptosis. Autophagy, a self-degradation system, controls apoptosis during stress conditions. However, to date, the mechanisms regulating the interplay between autophagy and apoptosis are still poorly understood. In this review, we summarize the current understanding of the molecular characteristics of autophagy in endometriosis and discuss future therapeutic challenges. Methods: A search of PubMed and Google Scholar databases were used to identify relevant studies for this narrative literature review. Results: Autophagy may be dynamically regulated through various intrinsic (e.g., PI3K/AKT/mTOR signal transduction network) and extrinsic (e.g., hypoxia and iron-mediated oxidative stress) pathways, contributing to the development and progression of endometriosis. Upregulation of mTOR expression suppresses apoptosis via inhibiting the autophagy pathway, whereas hypoxia or excess iron often inhibits apoptosis via promoting autophagy. Conclusion: Endometriotic cells may have acquired antiapoptotic mechanisms through unique intrinsic and extrinsic autophagy pathways to survive in changing environments.

Indexed as

apoptosisautophagyendometriosismitochondriamitophagy

Identifiers

PMID38645639
PMCPMC11031673
OpenAlexW4394980772

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.