Evidence map›Paper›PMID 36696012›Full record

ReviewCell stress & chaperones2023

The role of endoplasmic reticulum stress in endometriosis.

Hussein Riyadh Abdul Kareem Al-Hetty, Ahmed Darweesh Jabbar, Vladimir F Eremin, Abeer Mohsen Jabbar, Abduladheem Turki Jalil, Ali G Al-Dulimi, Hasanain A J Gharban, Muhammad Usman Faryad Khan, Marwan Mahmood Saleh

Open access · greenAbstract readReview
In one paragraph

Review in Cell stress & chaperones, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 8% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. 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

9 authors at 6 institutions in 2 countries.

Hussein Riyadh Abdul Kareem Al-HettyDepartment of Nursing, Al-Maarif University College, Ramadi, Iraq.
Ahmed Darweesh JabbarDepartment of Biology, College of Science, Wasit University, Al-Kut, Iraq.
Vladimir F EreminRepublican Scientific and Practical Center for Transfusiology and Medical Biotechnologies, Minsk, Belarus.
Abeer Mohsen JabbarCollege of Pharmacy, National University of Science and Technology, Nasiriyah, Dhi-Qar, Iraq.
Abduladheem Turki JalilDepartment of Medical Laboratories Techniques, Al-Mustaqbal University College, Hilla, Babylon, Iraq. abedalazeem799@gmail.com.ORCID 0000-0002-6513-2296
Ali G Al-DulimiDepartment of Dentistry, Bilad Alrafidain University College, Diyala, 32001, Iraq.
Hasanain A J GharbanDepartment of Internal and Preventive Veterinary Medicine, College of Veterinary Medicine, Wasit University, Al-Kut, Iraq.
Muhammad Usman Faryad KhanState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China.
Marwan Mahmood SalehDepartment of Biophysics, College of Applied Sciences, University of Anbar, Ramadi, Iraq.
University of Wasit · IQAlrafidain University College · IQAlsalam University College · IQSouthwest University · CNUniversity of Al Maarif · IQUniversity of Anbar · IQ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometriosis is a chronic gynecologic disorder characterized by abnormal growth of endometrium-like tissues in the ectopic regions of the pelvic peritoneum. The pathophysiology of endometriosis is not completely understood; however, excessive endometrial cell proliferation together with resistance to apoptosis facilitates the migration, implantation, and survival of endometrial cells in the distant sites. Endoplasmic reticulum (ER) stress response (also called unfolded protein response) is a cellular defense mechanism triggered by ER stress. When severe enough, the so-called response initiates cell suicide, i.e., apoptosis. Therefore, therapeutic induction of ER stress in endometriotic cells could promote apoptosis and contribute to the management of disease. In this review, we discuss the pathogenic role of ER stress in endometriosis and the most recent findings regarding the induction of ER stress in connection with endometriosis.

Indexed as

EndometriosisApoptosisEndometriumEndoplasmic Reticulum StressFemaleHumansUnfolded Protein ResponseEndometriosisEndoplasmic reticulum stressUnfolded protein responses

Identifiers

PMID36696012
PMCPMC10050460
OpenAlexW4317934433

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.