Evidence map›Paper›PMID 34974805›Full record

ArticleBioengineered2022

Extracellular vesicles derived from HBMSCs improved myocardial infarction through inhibiting zinc finger antisense 1 and activating Akt/Nrf2/HO-1 pathway.

Huiling Xiao, Dan Wu, Tao Yang, Wei Fu, Lu Yang, Chenkai Hu, Hongbing Wan, Xiaomin Hu, Chenjie Zhang, Tao Wu

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.9field-weighted citation impact, top 8% 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, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. The Potential of Mesenchymal Stem Cell-Derived Exosomes in Cardiac Repair.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Huiling XiaoDepartment of Cardiovascular Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Dan WuDepartment of medical technology, Jiangxi Health Vocational College, Nanchang, Jiangxi, China.
Tao YangDepartment of Emergency, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Wei FuDepartment of Emergency, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Lu YangDepartment of Cardiovascular Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Chenkai HuDepartment of Cardiovascular Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Hongbing WanDepartment of Cardiovascular Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Xiaomin HuDepartment of Cardiovascular Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Chenjie ZhangDepartment of Cardiovascular Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Tao WuDepartment of Cardiovascular Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.ORCID 0000-0002-9202-7029
Nanchang University · CNJiangxi Maternal and Child Health Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial infarction (MI) is believed to be one of the most common cardiovascular diseases, and it is seriously threatening the health of people in the world. The extracellular vesicles (EVs) isolated from mesenchymal stem cells and zinc finger antisense 1 (ZFAS1) have been believed to be involved in the regulation of MI, but the mechanism has not been fully clarified. Left anterior descending artery ligation was used to establish MI animal model, hypoxia treatment was applied to establish MI cell model. CCK8, transwell, and wound healing methods were applied to measure cell proliferation, invasion, and migration. Overexpression of ZFAS1 was established via transfecting pcDNA-ZFAS1. Overexpression of ZFAS1 significantly reversed the influence of EVs on cell migration, invasion, and apoptosis. Similar effect of EVs and ZFAS1 on morphological changes of MI rat heart tissues were also observed. The activation of Akt/Nrf2/HO-1 pathway by EVs was remarkably suppressed by pcDNA-ZFAS1. Inhibitor of Akt/Nrf2/HO-1 pathway remarkably reversed the impact of EVs on the cell viability. EVs might improve MI through inhibiting ZFAS1 and promoting Akt/Nrf2/HO-1 pathway. This study might provide a new thought for the prevention and treatment of MI damage through regulating ZFAS1 or Akt/Nrf2/HO-1 pathway.

Indexed as

Signal TransductionAnimalsCell HypoxiaCell MovementCell ProliferationCells, CulturedDisease Models, AnimalExtracellular VesiclesHeme Oxygenase (Decyclizing)HumansMaleMesenchymal Stem CellsMyocardial InfarctionMyocytes, CardiacNF-E2-Related Factor 2Proto-Oncogene Proteins c-aktHeme Oxygenase (Decyclizing)Hmox1 protein, ratNfe2l2 protein, ratNF-E2-Related Factor 2Proto-Oncogene Proteins c-aktRNA, Long NoncodingAktEVsHBMSCsHO-1Nrf2vWFZFAS1

Identifiers

PMID34974805
PMCPMC8805844
OpenAlexW4205621951

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.