Evidence map›Paper›PMID 38406291›Full record

ArticlePeerJ2024

Hypoxic bone marrow mesenchymal stem cell exosomes promote angiogenesis and enhance endometrial injury repair through the miR-424-5p-mediated DLL4/Notch signaling pathway.

Zhenghua Xiong, Yong Hu, Min Jiang, Beibei Liu, Wenjiao Jin, Huiqin Chen, Linjuan Yang, Xuesong Han

Open access · goldAbstract read
In one paragraph

Article in PeerJ, 2024. 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
6.4field-weighted citation impact, top 3% 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, 11 citations in OpenAlex.

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

8 authors at 5 institutions in 1 country.

Zhenghua Xiong *Department of Gynecology, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Yong Hu *Department of Gynecology, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Min JiangDepartment of Gynecology, Women and Children's Hospital Affiliated to Qingdao University, Qingdao, Shandong, China.
Beibei LiuDepartment of Gynecology, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Wenjiao JinDepartment of Gynecology, Yan'an Hospital Affiliated to Kunming Medical University/Yan'an Hospital of Kunming City, Kunming, Yunnan, China.
Huiqin ChenDepartment of Gynecology, Chuxiong Hospital of Traditional Chinese Medicine, Chuxiong, Yunnan, China.
Linjuan YangDepartment of Gynecology and Obstetrics, Baoshan Hospital of Traditional Chinese Medicine, Baoshan, Yunnan, China.
Xuesong HanDepartment of Gynecology, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
First Affiliated Hospital of Kunming Medical University · CNYan'an Hospital Affiliated To Kunming Medical University · CNBaoshan College · CNChuxiong Normal University · CNQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Currently, bone marrow mesenchymal stem cells (BMSCs) have been reported to promote endometrial regeneration in rat models of mechanically injury-induced uterine adhesions (IUAs), but the therapeutic effects and mechanisms of hypoxic BMSC-derived exosomes on IUAs have not been elucidated. Objective: To investigate the potential mechanism by which the BMSCS-derived exosomal miR-424-5p regulates IUA angiogenesis through the DLL4/Notch signaling pathway under hypoxic conditions and promotes endometrial injury repair. Methods: The morphology of the exosomes was observed Results: Compared with those in exosomes from normoxic conditions, miR-424-5p was more highly expressed in the exosomes from hypoxic BMSCs. Compared with those in normoxic BMSC-derived exosomes, the proliferation and angiogenesis of HUVECs were significantly enhanced after treatment with hypoxic BMSC-derived exosomes, and these effects were weakened after inhibition of miR-424-5p. miR-424-5p can target and negatively regulate the expression of DLL4, promote the expression of the proangiogenic genes Ang1 and Flk1, and inhibit the expression of the antiangiogenic genes Vash1 and TSP1. The effect of miR-424-5p can be reversed by overexpression of DLL4. In IUA rats, treatment with hypoxic BMSC exosomes and the miR-424-5p mimic promoted angiogenesis and improved endometrial damage. Conclusion: The hypoxic BMSC-derived exosomal miR-424-5p promoted angiogenesis and improved endometrial injury repair by regulating the DLL4/Notch signaling pathway, which provides a new idea for the treatment of IUAs.

Indexed as

ExosomesMesenchymal Stem CellsMicroRNAsUterine DiseasesAdaptor Proteins, Signal TransducingAngiogenesisAnimalsCalcium-Binding ProteinsFemaleRatsSignal TransductionAdaptor Proteins, Signal TransducingCalcium-Binding ProteinsMicroRNAsAngiogenesisBone marrow mesenchymal stem cellsDLL4/NotchEndometrial injuryHypoxic exosomesmiR-424-5p

Identifiers

PMID38406291
PMCPMC10894593
OpenAlexW4392085669

What OpenQuestion holds

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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.