Evidence map›Paper›PMID 35264108›Full record

ArticleBMC cardiovascular disorders2022

EZH2 mitigates the cardioprotective effects of mesenchymal stem cell-secreted exosomes against infarction via HMGA2-mediated PI3K/AKT signaling.

Wei Jiao, Jie Hao, Yanan Xie, Mingjie Meng, Weinian Gao

Open access · goldAbstract read
In one paragraph

Article in BMC cardiovascular disorders, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 22 citations in OpenAlex.

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  12. The role of PI3K signaling pathway in Alzheimer's disease.Frontiers in aging neuroscience · 2024
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  15. International journal of molecular sciences · 2023
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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

5 authors at 2 institutions in 1 country.

Wei JiaoDepartment of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei, People's Republic of China.
Jie HaoDepartment of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei, People's Republic of China.
Yanan XieDepartment of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei, People's Republic of China.
Mingjie MengDepartment of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei, People's Republic of China.
Weinian GaoDepartment of Cardiac Macrovascular Surgery, The Second Hospital of Hebei Medical University, No. 215, Heping West Road, Xinhua District, Shijiazhuang, 050000, Hebei, People's Republic of China. Gaown62104@126.com.
Hebei Medical University · CNSecond Hospital of Hebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMesenchymal stem cell-derived exosomes (MSC-EXO) have emerged as novel therapeutic strategies for myocardial infarction (MI). However, many questions remain untouched and unanswered regarding their roles in myocardial fibrosis. This study aimed to probe the therapeutic effects of MSC-EXO on myocardial fibrosis after MI and possible mechanisms.

methodsMyocardial tissues were obtained from MI rats, and myocardial cell viability, fibrosis, apoptosis, and epithelial-mesenchymal transition (EMT) were detected by immunohistochemistry, Masson's staining, TUNEL, and western blot. Bone marrow-derived MSCs and corresponding EXO were identified, and cardiac function were detected after treatment of MSC-EXO. Bioinformatics analysis and ChIP assay were conducted to detect the downstream genes of EZH2. EZH2 was upregulated alone or with HMGA2 overexpression in myocardial tissues of MI rats upon MSC-EXO treatment, and PI3K/AKT pathway activity in myocardial tissues was detected using western blot.

resultsThe proliferative activity in myocardial tissues of MI rats was significantly decreased, along with accentuated fibrosis, increased collagen volume and EMT. MSC-EXO treatment resulted in partial restoration of cardiac function and reduced EZH2 expression in the myocardium of rats. EZH2 inhibited HMGA2 expression by increasing the H3K27me3 modification. PI3K/AKT pathway was altered under the influence of the EZH2/HMGA2 axis. EZH2 inhibited the effect of MSC-EXO on the recovery of cardiac function and accelerated fibrosis, while HMGA2 reversed the effect of EZH2 to reduce fibrosis and enhance cardiac function.

conclusionMSC-EXO alleviated fibrosis in MI rats via inhibition of EZH2, whereas EZH2 inhibited HMGA2 expression and impaired the PI3K/AKT pathway.

Indexed as

ExosomesMesenchymal Stem CellsMyocardial InfarctionAnimalsEnhancer of Zeste Homolog 2 ProteinFibrosisHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanEZH2 protein, ratPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktEZH2HMGA2Mesenchymal stem cell-derived exosomesMyocardial fibrosisPI3K/AKT pathway

Identifiers

PMID35264108
PMCPMC8908676
OpenAlexW4221040177

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.