Evidence map›Paper›PMID 33907874›Full record

ArticleActa diabetologica2021

Long non-coding RNA KCNQ1OT1 increases the expression of PDCD4 by targeting miR-181a-5p, contributing to cardiomyocyte apoptosis in diabetic cardiomyopathy.

Shuo-Fang Zhao, Ying-Xian Ye, Jin-Dong Xu, Yi He, Deng-Wen Zhang, Zheng-Yuan Xia, Sheng Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Acta diabetologica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 2 pooled it
1.7field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Epigenetics in diabetic cardiomyopathy.Clinical epigenetics · 2024
    Review
  14. Construction of a potentially functional long noncoding RNA-microRNA-mRNA network in diabetic cardiomyopathy.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2024
    Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

7 authors at 3 institutions in 2 countries.

Shuo-Fang Zhao *Department of Anesthesiology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences and Guangdong Cardiovascular Institute, No.102, Zhongshan 2nd Road, Yuexiu District, Guangzhou, 510080, Guangdong Province, People's Republic of China.
Ying-Xian Ye *Department of Anesthesiology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences and Guangdong Cardiovascular Institute, No.102, Zhongshan 2nd Road, Yuexiu District, Guangzhou, 510080, Guangdong Province, People's Republic of China.
Jin-Dong XuDepartment of Anesthesiology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences and Guangdong Cardiovascular Institute, No.102, Zhongshan 2nd Road, Yuexiu District, Guangzhou, 510080, Guangdong Province, People's Republic of China.
Yi HeDepartment of Anesthesiology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences and Guangdong Cardiovascular Institute, No.102, Zhongshan 2nd Road, Yuexiu District, Guangzhou, 510080, Guangdong Province, People's Republic of China.
Deng-Wen ZhangDepartment of Anesthesiology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences and Guangdong Cardiovascular Institute, No.102, Zhongshan 2nd Road, Yuexiu District, Guangzhou, 510080, Guangdong Province, People's Republic of China.
Zheng-Yuan XiaDepartment of Anesthesiology, The University of Hong Kong, Pok Fu Lam, 999077, Hong Kong SAR, People's Republic of China.
Sheng WangDepartment of Anesthesiology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences and Guangdong Cardiovascular Institute, No.102, Zhongshan 2nd Road, Yuexiu District, Guangzhou, 510080, Guangdong Province, People's Republic of China. shenggg3@163.com.ORCID http://orcid.org/0000-0002-7789-5469
Guangdong Academy of Medical Sciences · CNTibet Autonomous Region People's Hospital · CNUniversity of Hong Kong · HK

Funding

Foundation for Basic and Applied Basic Research of Guangdong Province 2019A1515110063Guangdong Medical Research Fund A2020038Guangdong Natural Science Foundation 2018A030313535
6 · The paper itself

Abstract

aimsDiabetic cardiomyopathy (DCM) is a specific myocardial alteration in patients with diabetics. LncRNA KCNQ1OT1 has been previously demonstrated to be involved in various diabetic complications. Our aims are to further investigate the underlying regulatory mechanisms/pathways of KCNQ1OT1 in DCM.

methodsIn vitro and in vivo models of DCM were established in high glucose (HG)-treated human cardiomyocytes and in streptozotocin (STZ)-induced diabetic mice, respectively. Gene and protein expressions were examined by qPCR, western blotting and ELISA. Cell proliferation and apoptosis were determined by CCK8 assay, flow cytometry and TUNEL staining. The association between KCNQ1OT1 and miR-181a-5p, miR-181a-5p and PDCD4 was predicted using bioinformatics methods and subsequently confirmed by dual luciferase reporter and RNA immunoprecipitation assays. Mouse cardiac tissues were collected and analysed using HE staining, Masson's staining and immunohistochemical analysis.

resultsKCNQ1OT1 and PDCD4 were upregulated in HG-treated human cardiomyocytes, while miR-181a-5p was downregulated. In addition, KCNQ1OT1 could negatively regulate miR-181a-5p expression; meanwhile, miR-181a-5p also negatively regulated PDCD4 expression. KCNQ1OT1 silencing suppressed the expression of inflammatory cytokines and cell apoptosis in vitro, whereas inhibition of miR-181a-5p abrogated those effects of KCNQ1OT1 knockdown. Moreover, overexpressed PDCD4 abolished the inhibition on inflammation and apoptosis caused by miR-181a-5p overexpression. Finally, KCNQ1OT1 knockdown reduced the expression of PDCD4 via regulating miR-181a-5p and inhibited myocardial inflammation and cardiomyocyte apoptosis in the in vivo DCM model.

conclusionsOur findings suggest that KCNQ1OT1 and its target gene miR-181a-5p regulate myocardial inflammation and cardiomyocyte apoptosis by modulating PDCD4 in DCM.

Indexed as

Diabetes Mellitus, ExperimentalDiabetic CardiomyopathiesPotassium Channels, Voltage-GatedAnimalsApoptosisApoptosis Regulatory ProteinsHumansMiceMicroRNAsMyocytes, CardiacRNA-Binding ProteinsRNA, Long NoncodingApoptosis Regulatory ProteinsKCNQ1OT1 long non-coding RNA, humanMicroRNAsPDCD4 protein, humanPotassium Channels, Voltage-GatedRNA-Binding ProteinsRNA, Long NoncodingApoptosisDiabetic cardiomyopathyInflammationKCNQ1OT1MiR-181a-5pPDCD4

Identifiers

PMID33907874
OpenAlexW3158911581

What OpenQuestion holds

Textmetadata
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.