Evidence map›Paper›PMID 29218074›Full record

ReviewAmerican journal of translational research2017

Autophagy in endometriosis.

Hui-Li Yang, Jie Mei, Kai-Kai Chang, Wen-Jie Zhou, Li-Qing Huang, Ming-Qing Li

Open access · greenAbstract readReview
In one paragraph

Review in American journal of translational research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
5.4field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 66 citations in OpenAlex.

  1. Therapeutic Potential of Linalool in Endometriosis: Modulation of Oxidative Stress, Inflammation, and Apoptosis in a Rat Model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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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

6 authors at 3 institutions in 2 countries.

Hui-Li YangInsititute of Obstetrics and Gynecology, Hospital of Obstetrics and Gynecology, Fudan UniversityShanghai 200011, People's Republic of China.
Jie MeiDepartment of Obstetrics and Gynecology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical SchoolNanjing 210008, Jiangsu, People's Republic of China.
Kai-Kai ChangInsititute of Obstetrics and Gynecology, Hospital of Obstetrics and Gynecology, Fudan UniversityShanghai 200011, People's Republic of China.
Wen-Jie ZhouInsititute of Obstetrics and Gynecology, Hospital of Obstetrics and Gynecology, Fudan UniversityShanghai 200011, People's Republic of China.
Li-Qing HuangDepartment of Statistics and Psychology, College of Letters and Science, University of California DavisDavis, CA 95618, USA.
Ming-Qing LiInsititute of Obstetrics and Gynecology, Hospital of Obstetrics and Gynecology, Fudan UniversityShanghai 200011, People's Republic of China.
Fudan University · CNNanjing Drum Tower Hospital · CNUniversity of California System · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometriosis (EMS) is a common gynecologic disease that causes chronic pelvic pain, dysmenorrhea, and infertility in women. The doctrine of menstruation back flow planting and defects in the immune system are well known and widely accepted. In recent years, increasing studies have been focused on the role of autophagy in EMS, and have shown that autophagy plays a vital role in EMS. Autophagy, which is known as the non-apoptotic form of programmed cell death induced by a large number of intracellular/extracellular stimuli, is the major cellular pathway for the degradation of long-lived proteins and cytoplasmic organelles in eukaryotic cells. Autophagy commonly refers to macroautophagy, which is characterized by autophagosomes (double-membrane vesicles). In normal endometrial tissues, autophagy is induced in glandular epithelial and stromal cells throughout the menstrual cycle. However, aberrant autophagy occurs in the eutopic endometrium and ectopic endometriotic foci, which contributes to the pathogenesis of EMS by promoting the hyperplasia of endometriotic tissues and stromal cells, restricting apoptosis, and inducing abnormal immune responses. Consistent with changes in autophagy levels between normal endometria, eutopic and ectopic endometria from patients with EMS, the altered expression of autophagy-related genes (ATGs) is also observed. Currently, many factors are involved in the aberrant autophagy of endometriotic tissues, including female hormones, certain drugs, hypoxia, and oxidative stress. Therefore, studies focusing on autophagy may uncover a new potential treatment for EMS. The aim of this review is to discuss the role of aberrant autophagy in EMS and to explore the potential value of autophagy as a target for EMS therapy.

Indexed as

Autophagyautophagy-related genesendometrial stromal cellsendometriosis

Identifiers

PMID29218074
PMCPMC5714760
OpenAlexW2976648279

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.