Evidence map›Paper›PMID 33057899›Full record

ArticleGenes & genomics2020

LncRNA A2M-AS1 lessens the injury of cardiomyocytes caused by hypoxia and reoxygenation via regulating IL1R2.

Xue-Lian Song, Fei-Fei Zhang, Wen-Jing Wang, Xin-Ning Li, Yi Dang, Ying-Xiao Li, Qian Yang, Mei-Jing Shi, Xiao-Yong Qi

Abstract read
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Article in Genes & genomics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 18 citations in OpenAlex.

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  9. Epigenetic Signatures of Smoking in Five Brain Regions.Journal of personalized medicine · 2022
    Article
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  11. LncRNAs Target Ferroptosis-Related Genes and Impair Activation of CD4Frontiers in cell and developmental biology · 2021
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4 · The record

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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

9 authors at 2 institutions in 1 country.

Xue-Lian SongGraduate School, Hebei Medical University, Shijiazhuang, 050017, Hebei, People's Republic of China.
Fei-Fei ZhangDepartment of Cardiology Center, Hebei General Hospital, No. 348 of Heping West Road, Shijiazhuang, 050051, Hebei, People's Republic of China.
Wen-Jing WangDepartment of Cardiology Center, Hebei General Hospital, No. 348 of Heping West Road, Shijiazhuang, 050051, Hebei, People's Republic of China.
Xin-Ning LiDepartment of Cardiology Center, Hebei General Hospital, No. 348 of Heping West Road, Shijiazhuang, 050051, Hebei, People's Republic of China.
Yi DangDepartment of Cardiology Center, Hebei General Hospital, No. 348 of Heping West Road, Shijiazhuang, 050051, Hebei, People's Republic of China.
Ying-Xiao LiDepartment of Cardiology Center, Hebei General Hospital, No. 348 of Heping West Road, Shijiazhuang, 050051, Hebei, People's Republic of China.
Qian YangDepartment of Cardiology Center, Hebei General Hospital, No. 348 of Heping West Road, Shijiazhuang, 050051, Hebei, People's Republic of China.
Mei-Jing ShiDepartment of Cardiology Center, Hebei General Hospital, No. 348 of Heping West Road, Shijiazhuang, 050051, Hebei, People's Republic of China.
Xiao-Yong QiGraduate School, Hebei Medical University, Shijiazhuang, 050017, Hebei, People's Republic of China. youyouqiu88@126.com.
Hebei General Hospital · CNHebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyocardial ischemia and reperfusion injury (MI/RI) is a complex pathophysiological process, which can lead to severe myocardial injury. The long noncoding RNA alpha-2-macroglobulin antisense RNA 1 (A2M-AS1) has been revealed to be abnormally expressed in MI, However, its function in MI and the potential mechanism are still unclear.

objectiveTo evaluate the functional role of A2M-AS1 in hypoxia/reoxygenation (H/R)-induced neonatal cardiomyocytes and its potential molecular mechanism.

methodsDataset GSE66360 was obtained from GEO database for analyzing the RNA expression of A2M-AS1 and interleukin 1 receptor type 2 (IL1R2). KEGG pathway enrichment analysis of the genes that co-expressed with A2M-AS1 was performed. Human neonatal cardiomyocytes were subjected to H/R to construct in vitro models. QRT-PCR and Western blot were adopted to test the levels of mRNA and protein. The viability and apoptosis of cardiomyocytes were tested by CCK-8 and flow cytometry assays, respectively.

resultsThe expression of A2M-AS1 was notably downregulated in H/R-treated cardiomyocytes. Overexpression of A2M-AS1 can notably enhance the cell viability of H/R-damaged cardiomyocytes, whereas knockdown of A2M-AS1 showed the opposite outcomes. Besides, a negative correlation was showed between A2M-AS1 and IL1R2 expression. In H/R-treated cardiomyocytes, overexpression of IL1R2 weakened the promoting proliferation and anti-apoptosis effects caused by overexpressing A2M-AS1, however, IL1R2-knockdown abolished the anti-proliferation and pro-apoptosis effects caused by silencing A2M-AS1.

conclusionThis study demonstrates the potential regulatory role of A2M-AS1/ IL1R2 axis in cardiomyocytes suffered from H/R, and provides insight into the protection of MI/RI.

Indexed as

HypoxiaMyocardial ReperfusionApoptosisCell ProliferationCells, CulturedComputational BiologyGene Expression RegulationHumansMyocardial Reperfusion InjuryMyocytes, CardiacReceptors, Interleukin-1 Type IIRNA, Long NoncodingIL1R2 protein, humanReceptors, Interleukin-1 Type IIRNA, Long NoncodingAlpha-2-macroglobulin antisense RNA 1ApoptosisInterleukin 1 receptor type 2Myocardial ischemia and reperfusion injuryProliferation

Identifiers

PMID33057899
OpenAlexW3093118076

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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.