Evidence map›Paper›PMID 32790238›Full record

ArticleJournal of cellular and molecular medicine2020

MicroRNA-130a regulates neurological deficit and angiogenesis in rats with ischaemic stroke by targeting XIAP.

Wenjing Deng, Chenghe Fan, Yanan Zhao, Yuewei Mao, Jiajia Li, Yonggan Zhang, Junfang Teng

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 29% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. The influence of exercise duration on inhibiting endoplasmic reticulum stress in ischemic stroke rats.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
    Article
  3. Review
  4. Article
  5. MicroRNA Profiles in Critically Ill Patients.Current medicinal chemistry · 2024
    Review
  6. Angiogenesis after ischemic stroke.Acta pharmacologica Sinica · 2023
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. 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

7 authors at 2 institutions in 1 country.

Wenjing DengThe Neurology Intensive Care Unit, The First Affiliated of Zhengzhou University. Zhengzhou, Henan, China.
Chenghe FanThe Neurology Intensive Care Unit, The First Affiliated of Zhengzhou University. Zhengzhou, Henan, China.
Yanan ZhaoThe Neurology Intensive Care Unit, The First Affiliated of Zhengzhou University. Zhengzhou, Henan, China.
Yuewei MaoThe Vascular Surgery Department, Zhengzhou Central Hospital, Affiliated Hospital of Zhengzhou University. Zhengzhou, Henan, China.
Jiajia LiThe Neurology Department, Zhengzhou Central Hospital, Affiliated Hospital of Zhengzhou University. Zhengzhou, Henan, China.
Yonggan ZhangThe Vascular Surgery Department, The First Affiliated of Zhengzhou University. Zhengzhou, Henan, China.
Junfang TengThe Neurology Intensive Care Unit, The First Affiliated of Zhengzhou University. Zhengzhou, Henan, China.ORCID 0000-0001-5637-3701
First Affiliated Hospital of Zhengzhou University · CNZhengzhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) have already been proposed to be implicated in the development of ischaemic stroke. We aim to investigate the role of miR-130a in the neurological deficit and angiogenesis in rats with ischaemic stroke by regulating X-linked inhibitor of apoptosis protein (XIAP). Middle cerebral artery occlusion (MCAO) models were established by suture-occluded method, and MCAO rats were then treated with miR-130a mimics/inhibitors or/and altered XIAP for detection of changes of rats' neurological function, nerve damage and angiogenesis in MCAO rats. The oxygen-glucose deprivation (OGD) cellular models were established and respectively treated to determine the roles of miR-130a and XIAP in neuronal viability and apoptosis. The expression levels of miR-130a and XIAP in brain tissues of MCAO rats and OGD-treated neurons were detected. The binding site between miR-130a and XIAP was verified by luciferase activity assay. MiR-130a was overexpressed while XIAP was down-regulated in MCAO rats and OGD-treated neurons. In animal models, suppressed miR-130a improved neurological function, alleviated nerve damage and increased new vessels in brain tissues of rats with MCAO. In cellular models, miR-130a inhibition promoted neuronal viability and suppressed apoptosis. Inhibited XIAP reversed the effect of inhibited miR-130a in both MCAO rats and OGD-treated neurons. XIAP was identified as a target of miR-130a. Our study reveals that miR-130a regulates neurological deficit and angiogenesis in rats with MCAO by targeting XIAP.

Indexed as

AnimalsApoptosisBinding SitesBody WaterBrain ChemistryBrain Damage, ChronicCell HypoxiaCells, CulturedGene Expression RegulationGlucoseInfarction, Middle Cerebral ArteryInhibitor of Apoptosis ProteinsIntercellular Signaling Peptides and ProteinsMorris Water Maze TestNeovascularization, PhysiologicNeural Stem CellsGlucoseInhibitor of Apoptosis ProteinsIntercellular Signaling Peptides and ProteinsOxygenRNA, Small InterferingXiap protein, ratangiogenesisischaemic strokemicroRNA-130amiddle cerebral artery occlusionneurological deficitX-linked inhibitor of apoptosis protein

Identifiers

PMID32790238
PMCPMC7521252
OpenAlexW3048852187

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.