Evidence map›Paper›PMID 34239606›Full record

ArticleCardiovascular therapeutics2021

Downregulation of Long Noncoding RNA LINC00261 Attenuates Myocardial Infarction through the miR-522-3p/Trinucleotide Repeat-Containing Gene 6a (TNRC6A) Axis.

Chaoxin Jiang, Qing Zhao, Chenlong Wang, Minyan Peng, Guoqing Hao, Zhifeng Liu, Wenjin Fu, Kewei Zhao

Open access · goldAbstract read
In one paragraph

Article in Cardiovascular therapeutics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 40% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Role of LncRNAs in the Pathogenesis of Coronary Artery Disease.Reviews in cardiovascular medicine · 2023
    Review
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  6. Review
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 4 institutions in 1 country.

Chaoxin JiangDepartment of Clinical Laboratory, Guangdong Provincial Hospital of Integrated Traditional Chinese and Western Medicine, Foshan, Guangdong 528200, China.
Qing ZhaoDepartment of Clinical Laboratory, The Third Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510240, China.
Chenlong WangDepartment of Laboratory Medicine, Nanhai Hospital, Southern Medical University, Foshan, Guangdong 528244, China.
Minyan PengDepartment of Clinical Laboratory, Guangdong Provincial Hospital of Integrated Traditional Chinese and Western Medicine, Foshan, Guangdong 528200, China.
Guoqing HaoDepartment of Clinical Laboratory, Guangdong Provincial Hospital of Integrated Traditional Chinese and Western Medicine, Foshan, Guangdong 528200, China.
Zhifeng LiuDepartment of Clinical Laboratory, Guangdong Provincial Hospital of Integrated Traditional Chinese and Western Medicine, Foshan, Guangdong 528200, China.
Wenjin FuDepartment of Laboratory, Affiliated Houjie Hospital, Guangdong Medical College, Dongguan, Guangdong 523945, China.
Kewei ZhaoDepartment of Clinical Laboratory, The Third Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510240, China.ORCID https://orcid.org/0000-0003-4928-0026
Guangdong Provincial Hospital of Traditional Chinese Medicine · CNGuangzhou University of Chinese Medicine · CNGuangdong Medical College · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyocardial infarction (MI) is cardiac tissue necrosis caused by acute and persistent ischemic hypoxia of the coronary arteries. This study is aimed at investigating the expression of long noncoding RNA (lncRNA) LINC00261 in MI and its effect on myocardial cells.

methodsqRT-PCR was performed to detect the expression levels of LINC00261, miR-522-3p, and TNRC6A in normal and MI cells. Western blotting analysis was performed to detect the expression of TNRC6A protein. Viability and apoptosis of myocardial cells after MI with the knockout of LINC00261 or TNRC6A were detected. The relationships among miR-522-3p, LINC00261, and TNRC6A in cardiomyocytes were evaluated using a double luciferase reporter gene assay. Hypoxic preconditioning in normal cells was used to construct a simulated MI environment to investigate the effect of LINC00261 on apoptosis of cardiac cells.

resultsLINC00261 and TNRC6A were upregulated, while miR-522-3p was downregulated in coronary heart disease tissues with MI. Knockout of LINC00261 can increase the viability of cardiomyocytes and inhibit cell apoptosis. LINC00261 targets miR-522-3p in cardiomyocytes. In addition, miR-522-3p targets TNRC6A in cardiomyocytes. TNRC6A regulates cell viability and apoptosis of cardiomyocytes after MI, and TNRC6A-induced MI can be reversed by overexpression of miR-522-3p.

conclusionsLINC00261 downregulated miR-522-3p in cardiomyocytes after MI by directly targeting miR-522-3p. TNRC6A is the direct target of miR-522-3p. Our results indicated that LINC00261 might serve as a therapeutic target for the treatment of MI.

Indexed as

AnimalsApoptosisAutoantigensCell SurvivalDown-RegulationMaleMiceMice, Inbred C57BLMicroRNAsMyocardial InfarctionMyocytes, CardiacRNA-Binding ProteinsRNA, Long NoncodingUp-RegulationAutoantigenslong non-coding RNA 00261, humanMicroRNAsMIRN522 microRNA, humanRNA-Binding ProteinsRNA, Long NoncodingTNRC6A protein, human

Identifiers

PMID34239606
PMCPMC8235986
OpenAlexW3176768925

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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.