Evidence map›Paper›PMID 34645519›Full record

ArticleCell & bioscience2021

Chorionic villus-derived mesenchymal stem cell-mediated autophagy promotes the proliferation and invasiveness of trophoblasts under hypoxia by activating the JAK2/STAT3 signalling pathway.

Yijing Chu, Chengzhan Zhu, Chongyu Yue, Wei Peng, Weiping Chen, Guifang He, Changchang Liu, Yang Lv, Guoqiang Gao, Ke Yao and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

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  5. Importance of STAT3 signaling in preeclampsia (Review).International journal of molecular medicine · 2025
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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

14 authors at 1 institution in 1 country.

Yijing Chu *Department of Obstetrics and Gynaecology, The Affiliated Hospital of Qingdao University, 16 Jiangsu Road, Qingdao, 266000, China.
Chengzhan Zhu *Department of Hepatobiliary and Pancreatic Surgery, The Affiliated Hospital of Qingdao University, Qingdao, China.
Chongyu Yue *Department of Obstetrics and Gynaecology, The Affiliated Hospital of Qingdao University, 16 Jiangsu Road, Qingdao, 266000, China.
Wei PengDepartment of Obstetrics and Gynaecology, The Affiliated Hospital of Qingdao University, 16 Jiangsu Road, Qingdao, 266000, China.
Weiping ChenDepartment of Obstetrics and Gynaecology, The Affiliated Hospital of Qingdao University, 16 Jiangsu Road, Qingdao, 266000, China.
Guifang HeMedical Animal Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, China.
Changchang LiuMedical Animal Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, China.
Yang LvDepartment of Obstetrics and Gynaecology, The Affiliated Hospital of Qingdao University, 16 Jiangsu Road, Qingdao, 266000, China.
Guoqiang GaoDepartment of Obstetrics and Gynaecology, The Affiliated Hospital of Qingdao University, 16 Jiangsu Road, Qingdao, 266000, China.
Ke YaoDepartment of Obstetrics and Gynaecology, The Affiliated Hospital of Qingdao University, 16 Jiangsu Road, Qingdao, 266000, China.
Rendong HanDepartment of Obstetrics and Gynaecology, The Affiliated Hospital of Qingdao University, 16 Jiangsu Road, Qingdao, 266000, China.
Xiaoyu HuDepartment of Obstetrics and Gynaecology, The Affiliated Hospital of Qingdao University, 16 Jiangsu Road, Qingdao, 266000, China.
Yan ZhangDepartment of Obstetrics and Gynaecology, The Affiliated Hospital of Qingdao University, 16 Jiangsu Road, Qingdao, 266000, China. zhangyan78086@126.com.
Yuanhua YeDepartment of Obstetrics and Gynaecology, The Affiliated Hospital of Qingdao University, 16 Jiangsu Road, Qingdao, 266000, China. yeyuanhua8067@126.com.ORCID http://orcid.org/0000-0002-0517-0557
Qingdao University · CN

Funding

national natural science foundation of china 81600490postdoctoral science foundation of china 2019M652329, 2016M602098young taishan scholars program of shandong province 2019010668
6 · The paper itself

Abstract

backgroundTrophoblast dysfunction during pregnancy is fundamentally involved in preeclampsia. Several studies have revealed that human chorionic villous mesenchymal stem cells (CV-MSCs) could regulate trophoblasts function.

resultsTo understand how human chorionic villous mesenchymal stem cells (CV-MSCs) regulate trophoblast function, we treated trophoblasts with CV-MSC supernatant under hypoxic conditions. Treatment markedly enhanced proliferation and invasion and augmented autophagy. Transcriptome and pathway analyses of trophoblasts before and after treatment revealed JAK2/STAT3 signalling as an upstream regulator. In addition, STAT3 mRNA and protein levels increased during CV-MSC treatment. Consistent with these findings, JAK2/STAT3 signalling inhibition reduced the autophagy, survival and invasion of trophoblasts, even in the presence of CV-MSCs, and blocking autophagy did not affect STAT3 activation in trophoblasts treated with CV-MSCs. Importantly, STAT3 overexpression increased autophagy levels in trophoblasts; thus, it positively regulated autophagy in hypoxic trophoblasts. Human placental explants also proved our findings by showing that STAT3 was activated and that LC3B-II levels were increased by CV-MSC treatment.

conclusionIn summary, our data suggest that CV-MSC-dependent JAK2/STAT3 signalling activation is a prerequisite for autophagy upregulation in trophoblasts.

Indexed as

AutophagyChorionic villous-derived mesenchymal stem cellsJAK2/STAT3 signalling pathwayTrophoblasts

Identifiers

PMID34645519
PMCPMC8513187
OpenAlexW3205062203

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.