Evidence map›Paper›PMID 28783735›Full record

ArticlePloS one2017

The role of GPX1 in the pathogenesis of female pelvic organ prolapse.

Shasha Hong, Li Hong, Bingshu Li, Debin Wu, Cheng Liu, Jie Min, Wenjun Guo, Ming Hu, Jianming Tang, Yang Li

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Shasha HongDepartment of Obstetrics and Gynaecology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Li HongDepartment of Obstetrics and Gynaecology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.ORCID http://orcid.org/0000-0002-8081-1043
Bingshu LiDepartment of Obstetrics and Gynaecology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Debin WuDepartment of Obstetrics and Gynaecology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Cheng LiuDepartment of Obstetrics and Gynaecology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Jie MinDepartment of Obstetrics and Gynaecology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Wenjun GuoDepartment of Obstetrics and Gynaecology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Ming HuDepartment of Obstetrics and Gynaecology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Jianming TangDepartment of Obstetrics and Gynaecology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Yang LiDepartment of Obstetrics and Gynaecology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gestation and delivery can increase intra-abdominal pressure, which are well-known risk factors for Pelvic Organ Prolapse (POP). But the pathogenesis mechanism of POP remains unclear. Our previous research showed that the expression of glutathione peroxidase type 1 (GPX1) decreased in pelvic floor ligaments from POP patients, implying that oxidative stress (OS) may be related to POP. The aim of this study was to figure out the role of GPx1 regulation in the pathogenesis of POP. Women (>45 years) who received hysterectomy surgery were enrolled in this research, identified by screening. We applied mechanical strain of 0μ, 5333 μ to GPX1-overexpressing human uterosacral ligament fibroblasts (hUSLFs) isolated from menopausal women without POP respectively for 4 hours, in order to investigate the changes of cell apoptosis, oxidative status and ECM metabolism when cytomechanics model loaded on GPX1-overexpressing hUSLFs. Comparing with the non-transfection and mock-vehicle groups, we found that GPX1 not only protects hUSLFs from cell apoptosis, oxidative damage, but also improves the remodeling of ECM induced by mechanical stimulation. These results suggested that mechanical strain caused abnormalities of ECM metabolism via OS pathway in hUSLFs, which was involved in the pathogenesis of POP, and that GPx1 played a significant role in regulating mechanical strain induced POP.

Indexed as

ApoptosisBlotting, WesternCells, CulturedFemaleFibroblastsFlow CytometryGlutathione PeroxidaseGlutathione Peroxidase GPX1HumansLigamentsMiddle AgedOxidative StressPelvic Organ ProlapseReactive Oxygen SpeciesReverse Transcriptase Polymerase Chain ReactionGlutathione PeroxidaseGlutathione Peroxidase GPX1GPX1 protein, humanReactive Oxygen Species

Identifiers

PMID28783735
PMCPMC5546568
OpenAlexW2745054019

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.