Evidence map›Paper›PMID 32733638›Full record

ArticleOxidative medicine and cellular longevity2020

Exosomal CircHIPK3 Released from Hypoxia-Induced Cardiomyocytes Regulates Cardiac Angiogenesis after Myocardial Infarction.

Yan Wang, Ranzun Zhao, Changyin Shen, Weiwei Liu, Jinson Yuan, Chaofu Li, Wenwen Deng, Zhenglong Wang, Wei Zhang, Junbo Ge and 1 more

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

Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

60 citing papers in PubMed, 77 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

11 authors at 2 institutions in 1 country.

Yan WangDepartment of Cardiology, Affiliated Hospital of Zunyi Medical University, Zunyi 563000, China.ORCID https://orcid.org/0000-0001-8905-1055
Ranzun ZhaoDepartment of Cardiology, Affiliated Hospital of Zunyi Medical University, Zunyi 563000, China.
Changyin ShenDepartment of Cardiology, The Second Affiliated Hospital of Zunyi Medical University, Zunyi 563000, China.
Weiwei LiuDepartment of Cardiology, Affiliated Hospital of Zunyi Medical University, Zunyi 563000, China.
Jinson YuanDepartment of Cardiology, Affiliated Hospital of Zunyi Medical University, Zunyi 563000, China.
Chaofu LiDepartment of Cardiology, Affiliated Hospital of Zunyi Medical University, Zunyi 563000, China.
Wenwen DengDepartment of Cardiology, Affiliated Hospital of Zunyi Medical University, Zunyi 563000, China.
Zhenglong WangDepartment of Cardiology, Affiliated Hospital of Zunyi Medical University, Zunyi 563000, China.
Wei ZhangDepartment of Cardiology, Affiliated Hospital of Zunyi Medical University, Zunyi 563000, China.
Junbo GeDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Bei ShiDepartment of Cardiology, Affiliated Hospital of Zunyi Medical University, Zunyi 563000, China.ORCID https://orcid.org/0000-0001-5316-2351
Zunyi Medical University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exosomes play critical roles in mediating cell-to-cell communication by delivering noncoding RNAs (including miRNAs, lncRNAs, and circRNAs). Our previous study found that cardiomyocytes (CMs) subjected to hypoxia released circHIPK3-rich exosomes to regulate oxidative stress damage in cardiac endothelial cells. However, the role of exosomes in regulating angiogenesis after myocardial infarction (MI) remains unknown. The aim of this study was to establish the effects of exosomes derived from hypoxia-induced CMs on the migration and angiogenic tube formation of cardiac endothelial cells. Here, we reported that hypoxic exosomes (HPC-exos) can effectively reduce the infarct area and promote angiogenesis in the border surrounding the infarcted area. HPC-exos can also promote cardiac endothelial cell migration, proliferation, and tube formation in vitro. However, these effects were weakened after silencing circHIPK3 in hypoxia-induced CMs. We further verified that silencing and overexpressing circHIPK3 changed cardiac endothelial cell proliferation, migration, and tube formation in vitro by regulating the miR-29a expression. In addition, exosomal circHIPK3 derived from hypoxia-induced CMs first led to increased VEGFA expression by inhibiting miR-29a activity and then promoted accelerated cell cycle progression and proliferation in cardiac endothelial cells. Overexpression of miR-29a mimicked the effect of silencing circHIPK3 on cardiac endothelial cell activity in vitro. Thus, our study provides a novel mechanism by which exosomal circRNAs are involved in the communication between CMs and cardiac endothelial cells.

Indexed as

AnimalsCell HypoxiaCoronary VesselsExosomesMiceMice, Inbred C57BLMyocardial InfarctionMyocytes, CardiacNeovascularization, PhysiologicProtein Serine-Threonine KinasesRNA, CircularSignal TransductionTransfectionHipk3 protein, mouseProtein Serine-Threonine KinasesRNA, Circular

Identifiers

PMID32733638
PMCPMC7376438
OpenAlexW3042753181

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.