Evidence map›Paper›PMID 36785792›Full record

ArticleOxidative medicine and cellular longevity2023

MBNL1-AS1 Promotes Hypoxia-Induced Myocardial Infarction via the miR-132-3p/RAB14/CAMTA1 Axis.

Yanbing Li, Min Zong, Xiaonan Guan, Xuejiao Wu, Guiling Ma, Yu Wei, Zhi Li

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. 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.

Yanbing LiDepartment of Cardiology, Beijing Youan Hospital, Capital Medical University, Beijing 100069, China.
Min ZongDepartment of Cardiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Xiaonan GuanDepartment of Cardiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Xuejiao WuDepartment of Cardiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Guiling MaDepartment of Cardiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Yu WeiDepartment of Cardiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Zhi LiDepartment of Cardiovascular Medicine, the First Affiliated Hospital of Shantou University Medical College, Shantou, 515041 Guangdong, China.ORCID https://orcid.org/0000-0002-8856-039X
Capital Medical University · CNShantou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Mounting evidence have indicated that long noncoding RNA (lncRNA) muscleblind like splicing regulator 1 antisense RNA 1 (MBNL1-AS1) play a crucial regulatory role in cardiovascular disease, myocardial infarction (MI) included. In this research, we sought to probe into the biological function and potential mechanism of MBNL1-AS1 in MI. Methods: Cardiomyocytes were treated under hypoxic conditions for 0-12 h. Functional assays including CCK-8 and flow cytometry were performed to assess hypoxia-stimulated cardiomyocyte viability and apoptosis, respectively. Moreover, bioinformatics analysis and mechanical assays were conducted to reveal the competitive endogenous RNA (ceRNA) mechanism of MBNL1-AS1. Results: The upregulation of MBNL1-AS1 was found in hypoxia-stimulated cardiomyocytes. Functionally, the downregulation of MBNL1-AS1 dramatically promoted hypoxia-induced cardiomyocyte viability and inhibited apoptosis. Mechanistically, miR-132-3p bound to MBNL1-AS1 in hypoxia-induced cardiomyocytes, and miR-132-3p directly targeted RAB14, member RAS oncogene family (RAB14) and calmodulin binding transcription activator 1 (CAMTA1). Furthermore, MBNL1-AS1 upregulates the expression of RAB14 and CAMTA1 in hypoxia-stimulated cardiomyocytes via targeting miR-132-3p. Conclusions: The current study revealed the critical role of the MBNL1-AS1/miR-132-3p/RAB14/CAMTA1 axis in MI, indicating MBNL1-AS1 as an innovative therapeutic target for MI.

Indexed as

MicroRNAsMyocardial InfarctionApoptosisCalcium-Binding ProteinsCell ProliferationHumansHypoxiarab GTP-Binding ProteinsRNA, AntisenseRNA-Binding ProteinsTrans-ActivatorsCalcium-Binding ProteinsCAMTA1 protein, humanMBNL1 protein, humanMicroRNAsMIRN132 microRNA, humanRab14 protein, humanrab GTP-Binding ProteinsRNA, AntisenseRNA-Binding ProteinsTrans-Activators

Identifiers

PMID36785792
PMCPMC9922191
OpenAlexW4319171035

What OpenQuestion holds

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LicenceCC BY
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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.