Evidence map›Paper›PMID 36991356›Full record

ArticleBMC cardiovascular disorders2023

HOTAIR regulates SIRT3-mediated cardiomyocyte survival after myocardial ischemia/reperfusion by interacting with FUS.

Jixuan Liu, Mingzhuang Sun, Jinda Wang, Zhijun Sun, Gang Wang

Open access · goldAbstract read
In one paragraph

Article in BMC cardiovascular disorders, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 28% 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, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.

  1. LncRNAs as Emerging Diagnostic Biomarkers for Cardiovascular Diseases: Evidence Synthesis Through Systematic Review and Meta-Analysis.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
    Pooled it
  2. Review
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  4. Review
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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

5 authors at 4 institutions in 1 country.

Jixuan LiuDepartment of Cardiovascular, Beijing Friendship Hospital, Capital Medical University, No.95, Yongan Road, Beijing, 100050, China.
Mingzhuang SunDepartment of Cardiovascular, Aerospace Central Hospital, Beijing, 100853, China.
Jinda WangDepartment of Cardiology, The Sixth Medical Centre of PLA General Hospital, Beijing, 100853, China.
Zhijun SunDepartment of Cardiology, The Sixth Medical Centre of PLA General Hospital, Beijing, 100853, China.
Gang WangDepartment of Cardiovascular, Beijing Friendship Hospital, Capital Medical University, No.95, Yongan Road, Beijing, 100050, China. wg19820216@163.com.
Chinese PLA General Hospital · CNAerospace Center Hospital · CNBeijing Friendship Hospital · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyocardial ischemia/reperfusion (I/R) contributes to serious myocardial injury and even death. Therefore, prevention and mitigation of myocardial I/R is particularly important. LncRNA HOTAIR has been reported to be implicated in myocardial I/R progression. However, the detailed molecular mechanism of HOTAIR in cardiomyocyte was explored in myocardial I/R.

methodsFirstly, cell model of myocardial I/R was established through hypoxia/reoxygenation (H/R). Apoptosis and cell cycle were evaluated utilizing flow cytometry. The corresponding test kits were conducted to monitor the levels of LDH, Caspase3 and Caspase9. The gene expression and protein levels were detected by qPCR and western blot, respectively. RNA pull-down and RIP were performed to verify the interaction between FUS and lncRNA HOTAIR.

resultsIn AC16 cardiomyocytes treated with H/R, lncRNA HOTAIR and SIRT3 expression were obviously decreased. Overexpression of HOTAIR or SIRT3 could ameliorate H/R-induced cardiomyocyte injury by promoting cell viability, lowering LDH levels, and suppressing cell apoptosis. Further, lncRNA HOTAIR upregulated the expression of SIRT3 via interacting with FUS, thereby promoting the survival of H/R-injured cardiomyocytes.

conclusionLncRNA HOTAIR can improve myocardial I/R by affecting cardiomyocyte survival through regulation of SIRT3 by binding to the RNA binding protein FUS.

Indexed as

Coronary Artery DiseaseMyocardial IschemiaMyocardial Reperfusion InjuryRNA-Binding Protein FUSRNA, Long NoncodingSirtuin 3ApoptosisHumansMyocytes, CardiacFUS protein, humanHOTAIR long untranslated RNA, humanRNA-Binding Protein FUSRNA, Long NoncodingSIRT3 protein, humanSirtuin 3Cardiomyocyte survivalFUSlncRNA HOTAIRMyocardial ischemia/reperfusionSIRT3

Identifiers

PMID36991356
PMCPMC10061961
OpenAlexW4361280761

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.