Evidence map›Paper›PMID 34745428›Full record

ArticleOxidative medicine and cellular longevity2021

M1 Bone Marrow-Derived Macrophage-Derived Extracellular Vesicles Inhibit Angiogenesis and Myocardial Regeneration Following Myocardial Infarction via the MALAT1/MicroRNA-25-3p/CDC42 Axis.

Bairong Chen, Liyun Luo, Xiaoliang Wei, Dong Gong, Zhihui Li, Songbiao Li, Wenyi Tang, Lizi Jin

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 40 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Bairong ChenDepartments of Cardiovascular Disease IV, The Fifth Affiliated Hospital of Sun Yat-sen University, China.
Liyun LuoDepartments of Cardiovascular Disease I, The Fifth Affiliated Hospital of Sun Yat-sen University, China.
Xiaoliang WeiDepartments of Cardiovascular Disease IV, The Fifth Affiliated Hospital of Sun Yat-sen University, China.
Dong GongDepartments of Cardiovascular Disease IV, The Fifth Affiliated Hospital of Sun Yat-sen University, China.
Zhihui LiDepartments of Cardiovascular Disease IV, The Fifth Affiliated Hospital of Sun Yat-sen University, China.
Songbiao LiDepartments of Cardiovascular Disease IV, The Fifth Affiliated Hospital of Sun Yat-sen University, China.
Wenyi TangDepartments of Cardiovascular Disease IV, The Fifth Affiliated Hospital of Sun Yat-sen University, China.
Lizi JinDepartments of Cardiovascular Disease III, The Fifth Affiliated Hospital of Sun Yat-sen University, China.ORCID https://orcid.org/0000-0003-0397-9333
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial infarction (MI) is a severe cardiovascular disease. Some M1 macrophage-derived extracellular vesicles (EVs) are involved in the inhibition of angiogenesis and acceleration dysfunction during MI. However, the potential mechanism of M1 phenotype bone marrow-derived macrophages- (BMMs-) EVs (M1-BMMs-EVs) in MI is largely unknown. This study sought to investigate whether M1-BMMs-EVs increased CDC42 expression and activated the MEK/ERK pathway by carrying lncRNA MALAT1 and competitively binding to miR-25-3p, thus inhibiting angiogenesis and myocardial regeneration after MI. After EV treatment, the cardiac function, infarct size, fibrosis, angiogenesis, and myocardial regeneration of MI mice and the viability, proliferation and angiogenesis of oxygen-glucose deprivation- (OGD-) treated myocardial microvascular endothelial cells (MMECs) were assessed. MALAT1 expression in MI mice, cells, and EVs was detected. MALAT1 downstream microRNAs (miRs), genes, and pathways were predicted and verified. MALAT1 and miR-25-3p were intervened to evaluate EV effects on OGD-treated cells. In MI mice, EV treatment aggravated MI and inhibited angiogenesis and myocardial regeneration. In OGD-treated cells, EV treatment suppressed cell viability, proliferation, and angiogenesis. MALAT1 was highly expressed in MI mice, OGD-treated MMECs, M1-BMMs, and EVs. Silencing MALAT1 weakened the inhibition of EV treatment on OGD-treated cells. MALAT1 sponged miR-25-3p to upregulate CDC42. miR-25-3p overexpression promoted OGD-treated cell viability, proliferation, and angiogenesis. The MEK/ERK pathway was activated after EV treatment. Collectively, M1-BMMs-EVs inhibited angiogenesis and myocardial regeneration following MI via the MALAT1/miR-25-3p/CDC42 axis and the MEK/ERK pathway activation.

Indexed as

Animalscdc42 GTP-Binding ProteinExtracellular VesiclesFemaleMacrophagesMaleMiceMice, Inbred C57BLMicroRNAsMyocardial InfarctionMyocytes, CardiacNeovascularization, PathologicRNA, Long Noncodingcdc42 GTP-Binding ProteinCdc42 protein, mouseMalat1 long non-coding RNA, mouseMicroRNAsMIRN25 microRNA, mouseRNA, Long Noncoding

Identifiers

PMID34745428
PMCPMC8570847
OpenAlexW3210139912

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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.