Evidence map›Paper›PMID 27506466›Full record

ArticleScientific reports2016

Menopause-induced uterine epithelium atrophy results from arachidonic acid/prostaglandin E2 axis inhibition-mediated autophagic cell death.

Shengtao Zhou, Linjie Zhao, Tao Yi, Yuquan Wei, Xia Zhao

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 36 citations in OpenAlex.

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  8. The Multifaceted Role of Autophagy in Endometrium Homeostasis and Disease.Reproductive sciences (Thousand Oaks, Calif.) · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Shengtao ZhouDepartment of Gynecology and Obstetrics, Key Laboratory of Obstetrics &Gynecologic and Pediatric Diseases and Birth Defects of Ministry of Education, West China Second Hospital, and The State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, P. R. China.
Linjie ZhaoDepartment of Gynecology and Obstetrics, Key Laboratory of Obstetrics &Gynecologic and Pediatric Diseases and Birth Defects of Ministry of Education, West China Second Hospital, and The State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, P. R. China.
Tao YiDepartment of Gynecology and Obstetrics, Key Laboratory of Obstetrics &Gynecologic and Pediatric Diseases and Birth Defects of Ministry of Education, West China Second Hospital, and The State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, P. R. China.
Yuquan WeiDepartment of Gynecology and Obstetrics, Key Laboratory of Obstetrics &Gynecologic and Pediatric Diseases and Birth Defects of Ministry of Education, West China Second Hospital, and The State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, P. R. China.
Xia ZhaoDepartment of Gynecology and Obstetrics, Key Laboratory of Obstetrics &Gynecologic and Pediatric Diseases and Birth Defects of Ministry of Education, West China Second Hospital, and The State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, P. R. China.
Sichuan University · CNState Key Laboratory of Biotherapy

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Women experience menopause later in life. Menopause is characterized by dramatically decreased circulating estrogen level secondary to loss of ovarian function and atrophic state of genital organs. However, the molecular mechanisms for this process are not fully understood. In this study, we aimed to investigate the potential molecular mechanisms that underlie menopause-induced uterine endometrial atrophy. Our data showed that autophagy was activated in the uterine epithelial cells of both ovariectomized rats and peri-menopausal females. Endoplasmic reticulum (ER) stress occurred even prior to autophagy induction. Integrated bioinformatics analysis revealed that ER stress induced downstream decreased release of arachidonic acid (AA) and downregulation of AA/prostaglandin E2 (PGE2) axis, which led to Akt/mTOR signaling pathway inactivation. Consequently, autophagosomes were recruited and LC3-dependent autophagy was induced in uterine epithelial cells. Treatment with exogenous E2, PGE2, salubrinal or RNAi-mediated silencing of key autophagy genes could effectively counteract estrogen depletion-induced autophagy. Collectively, autophagy is a critical regulator of the uterine epithelium that accounts for endometrial atrophy after menopause.

Indexed as

AutophagyAnimalsArachidonic AcidAtrophyCells, CulturedDinoprostoneEndoplasmic Reticulum StressEpithelial CellsEpitheliumFemaleHumansMenopauseModels, AnimalProto-Oncogene Proteins c-aktRatsTOR Serine-Threonine KinasesArachidonic AcidDinoprostoneMTOR protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID27506466
PMCPMC4979008
OpenAlexW2503799317

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.